Statin drugs have been show to increase risk of death with a COVID-19 infection.
Tag: Diabetes
Why You Shouldn’t Worry About COVID-19 Any Longer
(Note: Author Updated this article on January 31, 2021)
I’ve been accused of writing this article because of my personal political motivation. That is not the case. I write this article because my patient’s expect me to treat them based on the actual science that exists, not the interpretative politics and non-evidence based health mandates that so many have recently cowered under, or used as a virtue signaling security blanket. A number of my patients, and potential patients, have notified me since I first published this article that I upset or angered them, because I haven’t conformed to “everyone else’s opinions.” My intent in writing this is not to anger anyone, agree with your opinion or to put forth a political agenda. Just because the media, politicians or city bureaucrats repeat something over and over doesn’t make it true. I share with you the actual science that has been recently made available so that you and I can make an educated judgement on how to act. Without an understanding of the actual evidence how are you and I to respond when there are so many voices sharing so many differing opinions? If you can’t trust your doctor to follow updated scientific evidence, then who can you trust?
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After graduation from medical residency, I served for four years as my AirForce Reserve unit’s biological/chemical weapons expert & physician. My job was to understand the risks of all the known biologic and chemical weapons that could be used on a human being, including severe viral and bacterial diseases that could pose a threat. My training was specifically focused on how to prevent and treat the effects of these illnesses in those under my care, military or otherwise.
I spent four years reading and researching where and when various types of masks, respirators and protective equipment would and should be used. Never once was a surgical or cloth mask ever found to be effective. Even N95 masks failed the rigors of these encounters.
This week our fearless Dr. Fauci says it’s “common sense” to wear two masks. So, my question to him and all of the other emperors of medicine is, what about three masks?
Even better yet, 10 masks makes even more “common sense!!” Where does this stop? (‘Cause my ears flop over at 11 masks.)
I’m thinking that 100 masks is 100% effective right?
I guess those filtered gas masks really aren’t essential then?!
One surgical mask decreases risk by 1-2% (yes, that’s the benefit of a mask that we’ve been required to wear). You’re more likely to have a 40% COVID risk reduction by throwing salt over your shoulder when you leave the house . . . (that’s the actual placebo effect).
The whole reason for mask wearing is to decrease “asymptomatic” transmission of COVID-19. That means, masks are supposed to decrease your risk of spreading or inhaling this virus when you or the person near you have no symptoms. Initially, we recommended wearing masks, because we did not know how infective the COVID-19 virus was to humans. We also knew that there was limited access to the N95 masks used in the hospital setting.
However, in the last 12 months, we’ve learned a great deal and we have a tremendous amount of data about treating this virus in the outpatient setting.
How Contagious is COVID-19?
What’s the actual risk of spreading the virus when you have no symptoms? It’s about 0.06% if you have prolonged contact (3 hours continuous face-to-face) with a person within six hours of that person having onset of symptoms (i.e. – fever, sore throat, fatigue, headache, loss of taste or smell, or runny nose). It is very rare to be infected at all with COVID-19 asymptomatically if you contact a person 6-9 hours before they have symptoms.
In fact, a recent study revealed there were no positive tests (or asymptomatic spread) among 1,174 close contacts of asymptomatic cases. So, why are we still wearing masks? Because it is politically convenient, increases fear, and increases your likelihood of getting a vaccine.
Are There Unintended Consequences of Mask Wearing?
Is wearing a mask to decrease a minimal risk by 1% more worth the risk? Increased bacterial and fungal infections that are on the rise as a consequence of chronic and continued daily mask wearing.
I’m seeing patients with increased frequency of facial rashes, fungal infections, non COVID-19 induced bacterial infections. Reports are coming from my colleagues, all over the world, that suggest bacterial pneumonias are on the rise.
Why? Because we are wearing and re-wearing of dirty masks. Untrained members of the public are wearing medical masks, repeatedly… in a non-sterile fashion… They’re becoming contaminated. They’re pulling them off of their car seat, off the rearview mirror, out of their pocket, from their countertop, and they’re reapplying a mask that should be worn fresh and sterile every single time. And, there is no way around this when 330 million people are required to wear a mask to go to Wal-Mart or Costco.
In a recent report in Emerging Infectious Diseases, the U.S. Centers for Disease Control and Prevention (CDC) suggests what experts have stated all along: There is no conclusive evidence that cloth masks protects users from coronavirus, especially since most people do not use them correctly and do not keep them clean.
The report actually says, “To our knowledge, only 1 randomized controlled trial has been conducted to examine the efficacy of cloth masks in healthcare settings, and the results do not favor use of cloth masks. More randomized controlled trials should be conducted in community settings to test the efficacy of cloth masks against respiratory infections.”
So, why, again, are we wearing these masks?
Should We Still Be Hiding In Our Homes?
Six months after the the largest variant of the five coronavirus sub-types appeared with it’s ugly little glycoprotein envelope and infective RNA fusion peptide coating, many states and countries are still in a quarantine or lock-down. Initially, because of the rapid infection rate that was seen in Italy and China, health experts recommended quarantine of the general population in order to keep hospital systems and medical providers from being overwhelmed. However, the “overwhelm” has been quite underwhelming. This begs answer to four very important questions:
- Should we still be quarantined?
- Should we still be wearing a mask when in public?
- Should businesses still be shut down?
- Should we wait for a vaccine?
This is the first time in history that large scale quarantine of the healthy across the country was ever used. The sole purpose was to control the number of severe cases requiring intensive care and ventilator use. Multiple mathematical models predicted that hundreds of thousands would die based upon statistics seen in Italy and China.
In early February, 2020, we were concerned that risk of death as high as 5.5% in our initial data from Italy and China. Limited N95 masks and protective equipment was available. In agreement with the CDC and WHO, I recommended everyone wear a mask, take drastic infection precautions and quarantine to prevent risk of transmission (Davies A, et al., Aug 2013).
Because viruses like COVID-19 and influenza are so small, a single layer cloth mask and or surgical mask has only been shown to decrease your risk of viral infection or transmission to others by 1-2%. Triple layer cloth masks with central interfacing layer give 3% – 20% reduction of infection risk based on the studies we have in the medical literature (Disaster Med Public Health Preparedness. 2013;7:413-418). At the time we learned about this virus, our understanding was that any protection was better than no protection.
Underwhelming
Yet, as this virus crossed our shores, traveled over the amber waves of grain and ascended the majestic purple mountains of majesty, the overwhelming number of patients hitting the hospital in droves isn’t what we saw. A few areas like New York and Washington State were hit hard, but not nearly as predicted. The large numbers of deaths seen in these states is because of their decision to send thousands of recovering COVID-19 patients into nursing homes, exposing those over 65 at greatest risk for death, to this virus.
Some claim that this is because we quarantined the healthy, yet if this were the case, infections would begin to rise as soon as lock-downs were lifted. Yet, no surge has come in the last three to four weeks, not even a blip. And Sweden, who only quarantined the sick and the elderly at high risk, has not seen the overwhelming surge of death so many predicted.
As of June 18th, eight weeks from the time we began opening up businesses, elective surgeries and letting people go back to work, the death count from COVID-19 continued to fall. If social distancing and mask wearing was really effective, significant rise in infections and COVID-19 deaths should have escalated in mid-May (5-6 days after exposure). Yet, in states like Arizona COVID-19 death counts continued to fall.
Quarantine of the Healthy
In all of history, we have never seen any benefit to quarantining the healthy. In fact, quarantine of the healthy has been demonstrated to be unhealthy for a “well population” (Brooks SK, et al., Lancet, Feb 2020). Based on scientific evidences we have today, despite what our politicians say, there is no reason to quarantine those that are not ill. Seeing all this data over the last two weeks dramatically changed my perspective on this virus.
Asymptomatic Transmission
“Oh no, Dr. Nally! You can’t say that, because this virus can be transmitted when you’re not symptomatic!” Yes. I’ve heard that argument for the last three months. And it is unfounded.
The main reason for quarantine was the fear of asymptomatic transmission. Early editorial reports (these were not actually controlled studies, they were opinion reports based on a case review) showed that the virus “may” be spread prior to a person showing symptoms via respiratory secretions. Initial data in seven very small presumptive editorial case reports out of China, Singapore and Germany postulated that this could occur in 40-50% of those infected (1,2,3,4,5,6,7). Yet all of these articles were case reports of 1-10 people and the exact mechanism of transmission was observational only and is still unknown.
The CDC made its recommendations on wearing masks based on these seven presumptive editorial cases between January and May, 2020. Recent nursing home case report data from April and May looked at 76 people in two nursing homes, 50% of those with positive infections were asymptomatic for the first 5-6 days. The report implies that those with COVID-19 must have had the potential to spread the disease 3-4 days before onset of symptoms. All of our social distancing and mask wearing has been based on upon these seven very small presumptive case reports and/or medical editorials. Never in medical history has sweeping health recommendations or mandates been made on editorial reports alone.
It is very important to note a recent larger population study of 455 patients was performed looking at infected members of families and those living in close quarters over 2-4 weeks. The researchers findings were opposite that of the seven small case reports above and concluded that the likely hood of asymptomatic SARS-CoV-2 transmission was “weak.”
The assumption that viral infections can be transmitted in the asymptomatic state comes from the Ghandi study, and others, that 30-50% of asymptomatic influenza patients can spread the flu a full 3-4 days prior to showing any symptoms, and in some cases up to 7 days prior to symptom onset. We’ve assumed that is the case with COVID-19, but that isn’t what the larger study demonstrated.
Have we or do we currently quarantine the healthy or institute social distance because of asymptomatic influenza spreading risk? No.
Do we quarantine the healthy or social distance because of the highly contagious croup or whooping cough (that is still prevalent on our southern border)? No.
But, these are the same editors and journals that have been telling us for the last 50 years that eating fat makes us fat. So, we must trust them, right? Wait, didn’t the New England Journal of Medicine and the Lancet both just retract “ground breaking” articles on COVID-19 because of falsified data that was never peer reviewed?
The fear of asymptomatic spread is therefore a mute point, as it is roughly identical to the flu. And it has infectious similarities to other infectious diseases like whooping cough (pertussis) and the croup (para-influenza virus). If the only actual large study of COVID-19 demonstrates that asymptomatic droplet based spread is weak, then why have we created fear and economic collapse for a virus that is less likely to spread in the asymptomatic person than the flu, croup, or whooping cough?
Risk Factor for Disease Severity
These three maladies (hypertension, diabetes & coronary artery disease) are the three most common medical problems that I see in my clinic, and they affect 85% of the people in my practice. All three are caused and driven by hyperinsulinemia.
Hyperinsulinemia is defined as an elevated insulin production (2-30 times normal) when ingesting any form of carbohydrate or starch. It starts 15-20 years before the onset of diabetes and is the cause of hypoglycemia, elevated fasting blood sugar, pre-diabetes, metabolic syndrome, chronic kidney disease, idiopathic neuropathy, hypertension and coronary artery disease.
Elevated insulin, even small elevations, puts a load on the immune system. The higher your insulin response to starches or sugars, the more likely you are to have hypertension, diabetes and heart disease. We found that those with elevated insulin levels and those over 45 years old with stressed immune systems are the most susceptible to severe COVID-19 infection.
We know that those who do get severely ill are those over 45 with immune system compromise and/or hyperinsulinemia. A very interesting fact was published in The Lancet. The authors found that the highest rates of death occurred in those with current hypertension, diabetes and/or coronary artery disease (heart disease or atherosclerosis of the arteries).
Interestingly, Italy, Spain and Portugal have the highest incidence of metabolic syndrome (hyperinsulinemia) across all of Europe. It stands to reason that they have also been hit the hardest with a virus that is focused on this form of immune-compromise.
Corona-Virus is Quite Common
The corona-virus, traditionally, causes a simple common cold. In fact, 2% of the population are asymptomatic carriers of the six corona-virus strains that are known to infect humans. And this class of virus is responsible for 10% of respiratory infections yearly around the world (Cascella M, et al. 2020 Apr 6. In: StatPearls.).
Should We Still Be In Quarantine?
Should we still be in quarantine? The answer is therefore “no.”
What we should be focused on is limiting exposure to those with the greatest risk like those in nursing homes, care centers, populations of elderly (over 65 years old), and those with known risk for suppressed immunity. Our focus, efforts and funds should be spend keeping these populations from exposure to COVID-19.
Should we still be wearing masks in public?
As noted above, cloth masks provide only very minimal (20-40%) protection from bacteria and almost no protection (1-2.3%) from viral infections. The two studies that do exist about effectiveness of mask wearing during viral infections to prevent spread demonstrate that adherence is very difficult and that transmission of viral infections is not statistically different between those wearing masks and those not wearing masks (MacIntyre CR et al., Cowling BJ et al.). Because we now know that this virus is similar to influenza in risk for death, general healthy populations should have no need to wear masks. Wearing of a mask actually increases the likely-hood of infection by increased frequency of touching your face. It also perpetuates a climate of risk and fear. It, also, implies that if required, mask should be a covered cost of medical provision at the State and Federal levels. As you can see, even the NIH director over NIAID, Anthony Fauci, MD, the one person in the country with the most experience in pandemic infectious disease, has trouble wearing a mask in public.
Second, there are a number of other medical problems including exacerbation of headache and migraines that occurs with chronic use of both surgical and N95 masks. For those who have COPD, mask wearing can exacerbate hypercapnia (increased carbon dioxide levels causing slowed respiration, confusion and fatigue). Mask wearing can also cause chronic hypoxia (reduced oxygenation) which has been shown to increase risk of cancer growth. In cases where patients with pulmonary fibrosis or impaired lung function wear masks for prolonged periods, syncope or loss of consciousness has been documented.
Therefore, wearing a mask for prolonged periods of time when it is not medically justified is not recommended and in many cases dangerous to your health.
Despite this, and the fact that there is significant doubt as to asymptomatic transmission of this virus, mandates to wear face masks in public were decreed across Arizona today.
Should businesses be shut down?
If our ultimate goal was to “flatten the curve,” and protect hospitals from being overwhelmed, then we were successful at doing that in mid-April. Some communities rightfully extended that quarantine to the end of April. However, there has been no justifiable evidence to suggest that healthy people cannot go back to work, feed their families, pay their mortgages and provide for themselves. In fact, multiple states including Wisconsin, Kansas, & Michigan have had Federal courts overturn draconian quarantine measures enacted by over-reaching emergency gubernatorial orders.
How accurate are the tests anyway?
The accuracy and predictive values of SARS-CoV-2 tests have not been systematically evaluated, and the sensitivity of testing likely depends on the precise RT-PCR assay, the type of specimen obtained, the quality of the specimen, and duration of illness at the time of testing.
In a study of 51 hospitalized patients in China with positive SARS-CoV-2 RT-PCR test (mainly on throat swabs), 15 patients (29 percent) had a negative initial test and only were diagnosed by serial testing [Fang Y, et al., Radiology 2020]. In a similar study of 70 patients in Singapore, initial nasopharyngeal testing was negative in 8 patients (11 percent) [Lee TH, et al. Clin Inf Dis 2020]. In both studies, rare patients were repeatedly negative and only tested positive after four or more tests.
Seven additional studies (including two unpublished reports) that evaluated RT-PCR performance, the estimated rates of false-negative results were 100 percent on the day of exposure, 38 percent on day 5 (estimated as the first day of symptoms), 20 percent at day 8, and 66 percent at day 21 [Kucirka LM, et al., Ann Int Med 2020].
And even though manufacturers are pushing the new antibody testing, antibody testing with IgG and/or IgM tests are frequently falsely positive [Guo L, et al., Clin Infect Dis 2020] and have been shown to be erroneous 20-30% of the time. The accuracy and time to antibody detection vary with the particular test used. Studies evaluating the specificity of serologic tests in a broad population are lacking; in particular, the rate of cross-reactivity with other coronaviruses is a potential concern, and IgM tests are prone to false-positive results.
In the first week since symptom onset, fewer than 40 percent had detectable antibodies; by day 15, IgM and IgG were detectable in 94 and 80 percent, respectively.
In the United States, several serologic tests have been granted emergency use authorization by the FDA for use by laboratories certified to perform moderate- and high-complexity tests [FDA.gov]. The FDA highlights that serologic tests should not be used as the sole test to diagnose or exclude active SARS-CoV-2 infection. The sensitivity and specificity of many of these serologic tests are uncertain.
Should We Wait For A Vaccine?
As a preface to this section, please be aware that I am a very strong proponent of safe and effective vaccine use. Because the RNA vaccines are so new, long-term efficacy, safety and adverse reaction studies are essential before these vaccines can be recommended across the board. It takes at least 4-5 years to 1) bring a vaccine to market and 2) complete adequate safety studies.
Let’s start by looking at the effectiveness of current RNA viral vaccines. The most common RNA vaccine currently in use is the influenza vaccine, quadravalent (four flu strains) and high dose (five flu strains) versions. Over the last 20 years, the percentage of seniors getting flu shots increased sharply from 15% to 65%. It stands to reason that flu deaths among the elderly should have taken a dramatic dip due to increased flu vaccination each year.
Instead, as you can see above, influenza deaths among the elderly continued to climb. It was hard to believe, so researchers at the National Institutes of Health set out to do a study adjusting for all kinds of factors that could be masking the true benefits of the shots. But no matter how they crunched the numbers, they got the same disappointing result: flu shots had not reduced deaths among the elderly.
It’s not what health officials hoped to find. I was shocked when I read these studies. Two studies, here and here, demonstrate that yearly flu vaccine for those over age 65 does nothing to decrease influenza related death. These studies funded by the government in 2005 and 2006 were suppressed and I never heard about them. Yet the CDC still emphasizes to the elderly, “Get your flu shot.”
One reason these vaccines are ineffective is that viruses like influenza and corona-viruses are highly antigenic. That means that there are hundreds of strains and the virus is changing rapidly. Influenza has over 600 strains. Our current high dose vaccine only covers five of these strains.
SARs-CoV-2 (COVID-19) is known to have over 160 strains. “There are too many rapid mutations to neatly trace a COVID-19 family tree.” Said Peter Forster, geneticist at the University of Cambridge. “We used a mathematical network algorithm to visualize all the plausible trees simultaneously.” (Proceedings of the National Academy of Sciences, 2020). Dr. Forster’s research identifies 160 genomes within the hundreds of additional variants of the three central COVID-19 strain variants.
The other very fascinating concern found when making RNA virus vaccines is the potential to increase susceptibility to other viruses. In a Department of Defense study, looking at 6000 military personal vaccinated in the 2017-2018 season, those who got the influenza vaccine demonstrated an increases susceptibility to corona-viruses by 36%. Those who were vaccinated with the flu vaccine had additional increased susceptibility to non-influenza viruses by 15%, and increased susceptibility to human metapneumovirus by 59%.
A second influenza study demonstrated an increased risk of para-influenza virus in adults (increased by 4.6% of vaccinated adults and only 2.6% of unvaccinated adults.) Though the researchers dismissed it as calculation error, the p value reflects that the vaccine played some roll (P=0.04) in the increased susceptibility.
Herd Immunity? Maybe in 200 Years
Do the math on a vaccine that covers only four out of 600+ strains like the quadravalent influenza vaccine. For a vaccine to create “herd immunity,” currently being touted across the airwaves as the way to return to normal, it would require the average human to be vaccinated every year for 100 years, and would take 200-400 years to create any semblance of herd immunity. And, that’s after 4-5 years studying the safety of a vaccine in large populations.
Influenza and HPV, the two most widely used RNA vaccines, still have a number of post-market adverse reactions including: Guillain-Barré syndrome (GBS), convulsions, febrile convulsions, myelitis (including encephalomyelitis and transverse myelitis), facial palsy (Bell’s palsy), optic neuritis/neuropathy, brachial neuritis, syncope (shortly after vaccination), dizziness, and paresthesia (tingling of the extremities) (Package-Insert—Gardasil.pdf; Package-Insert—Fluzone High Dose.pdf). Though these adverse events occur more rarely, it is essential you and I understand the risks of these newer RNA vaccines.
Conclusion
In summary, our focus should be shifting to protecting our elderly and immune-compromised. The evidence does not support quarantine of the healthy. Evidence does not support general public mask wearing. And there is no evidence that continued business closure is beneficial.
What can you and I do?
- Reduce your risk of hyperinsulinemia. Follow a carbohydrate restricted diet, exercise, control blood sugar, blood pressure, cholesterol and limit risk factors that suppress your immune system. Quit smoking, vaping, etc.
- Actively engage your congressman or congresswoman. What are they are doing to assist/protect the seniors, nursing home patients, and shut-in’s in your area?
- Let your governor or mayor hear your voice. What damage has quarantine has done to your livelihood and those of your family?
- Get educated about your civil liberties and do not let anyone take them under the guise of an emergency.
- Ensure your loved ones, especially the elderly and immune suppressed, understand the truth about their risk of infection.
Don’t be afraid to go outside and be a human being again.
Why Salt is So Important on a Ketogenic Diet?
The most common complaint that I get in my office when someone has started a ketogenic diet is, “Doc, I feel fatigued. Will this ever go away?”
That feeling of fatigue, some refer to as the “keto-flu,” is usually due to a couple of things. First, you may not be eating enough fat (I recommend a 1 gram to 1 gram ratio of protein to fat when getting started). Second, you’re not taking in enough salt (specifically sodium, potassium, magnesium and/or zinc). These four salts are essential electrolytes our body requires for proper function.
If salt is the problem, the you will be experiencing leg cramps. Cramps during daytime activity are usually due to low sodium or potassium levels. Cramps that wake you up at night are usually due to low magnesium or zinc. Leg cramps can also be due to hypothyroidism or significant blood sugar swings. Dr. Nally will usually check for this during your visit with him.
“But isn’t too much salt bad for you?” I am frequently asked.
Too much salt is only bad for you if you’re eating a “low-fat” diet.
What if increasing salt intake actually lowered your blood pressure?
Did you know that increasing your salt intake can actually improve your diabetic blood sugar if you are following a correct diet? Could it be that easy?
Almost every patient that I see in the office has a significant worry about salt intake, some greater than others. In fact, some people are so fearful about salt that when I initially began encouraging its use, they told me that I was crazy, and they left my practice.
Has restricting salt over the last 50 years really worked, or is it doing more damage than we think?
That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago. However, his answer never got a mention. In fact, I’ve been in practice for almost 20 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, the study is a small sample size of people, only twenty-one. However, the results are profound.
Twenty-one patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day). Glucose tolerance tests were completed with insulin levels at the end of each intervention period.
Insulin Resistance and Hypertension Improve by Adding Salt
Three very noteworthy results happened. First, those patients with insulin resistance and diabetes had improvement in their glucose levels while on 2 grams of sodium supplementation.
Second, those with hypertension also, shockingly, showed improvement in their blood pressure while on the 2 grams of sodium supplementation.
Third, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake. These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”
“But, Dr. Nally, you can’t base your findings on a small group of 21 people,” the experts say.
Yes, it is a small study group. However, these findings are identical to what I, also, see clinically every day in my practice for over 20 years.
We know that the average human needs at a minimum 3 grams of sodium per day and 3 grams of potassium per day. The standard American diet (SAD diet) including processed foods contains 2-3 grams per day of sodium and potassium. In fact, the CDC claims the worst salt containing meals for you are:
- Bread
- Processed chicken dinners
- Pizza
- Pasta
Insulin also stimulates additional retention of sodium at the kidney level. If you are insulin resistant, producing excess insulin in response to starches or sugars, you retain notably larger amounts of salt when eating the standard American diet (SAD diet) or a “low-fat” diet. However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt.
Salts, or electrolytes, are essential in normal cellular function. Low salt in the body is like running your car without oil. It will run, but not very efficiently and over the long term will cause problems. This is the cause of the keto-flu I wrote about previously. And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.
How Much Salt Should I Use?
In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle. That’s approximately 1 ½ – 2 teaspoons of salt per day. I like the Redmond’s RealSalt or pink Himalayan salt because these products contains all four types of salt (sodium, potassium, magnesium and zinc).
It is probably that your salt restrictions is making your insulin resistance and blood pressure worse. That’s what the clinical evidences are pointing toward, and it is what I see every day in my office.
Want to know more about a ketogenic life-style? Click the KetoLife link to get some basics.
If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the KetoKart and checking out the products I recommend to jump-start ketosis DocMuscles-style!
Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!
What If Salt Actually Improves Blood Pressure & Blood Sugar?
What if increasing your salt intake actually improved your diabetic blood sugar?
What if increasing salt intake actually lowered your blood pressure? Could it be that easy?
Just about every patient that I see has significant worry about salt intake. Some greater than others. In fact, some people are so salt phobic that when I encouraged its use, they called me a “quack” and left my practice. But does salt restriction really work, or is it doing more damage than we think?
That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago. However, his answer never got a mention. In fact, I’ve been in practice for almost 18 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, it is a small sample of people, only 21 in the study. However, the results are profound.
21 patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day). Glucose tolerance tests were completed with insulin levels at the end of each intervention period.
Insulin Resistance and Hypertension Improve by Adding Salt
What was noteworthy was that those with insulin resistance and diabetes had improvement in their glucose levels while on sodium supplementation. Those with hypertension had improvement in their blood pressure while on the sodium supplementation. Lastly, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake. These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”
“But, you can’t base your findings on a small group of 21 people,” the experts say.
Yes, it is a small study group. However, these findings are what I, also, have seen clinically in my practice for over 13 years.
We know that the average human needs 3 grams of sodium per day and 3 grams of potassium per day. If you’re eating the standard American diet (SAD diet) including processed foods, you’re getting 2-3 grams per day of sodium. In fact, the CDC claims the worst meals for you are:
- Bread
- Processed chicken dinners
- Pizza
- Pasta
However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt. This is the cause of the keto-flu I wrote about a few weeks ago. And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.
How Much Salt Should I Use?
In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle. That’s approximately 1 1/2 – 2 teaspoons of salt per day. I like Redmond’s RealSalt or if you can’t find it, Himalayan Pink Salt, because the pink sea salts contain sodium, potassium, magnesium and zinc.
Could it be that salt restrictions are making our insulin resistance and blood pressure worse? That’s what the clinical evidences are pointing toward. However, more research is still needed.
Want to know more about a ketogenic life-style? Click the link on KetoLife above to get some basics. If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the Supplement section above and checking out the products I recommend to jump-start ketosis DocMuscles style!
Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!
Ketones – One of the Keys to the Fat Lock-Box
Do you have the keys to your “fat lock-box?”
Lock-boxes have always fascinated me. Lock-boxes with special keys are even more fascinating. The more I’ve learned about fat cells (adipocytes), the more I think about them as special fuel depositories or fat lock-boxes. Before the invention of refrigerators, fast-food, Bisquick and beer, our bodies preserved and reserved fat as a precious commodity.
The body, when given fat with carbohydrates or excess protein, quickly places the fat into a lock-box for safe keeping. It does this for two reasons. First, the body can store fat very efficiently. Second, hormone signals stimulate fat storage when other fuel sources (carbohydrate & protein) are present in excess. The body can access this stored fuel only when the right presentation of hormonal keys are present. Fascinatingly, we now know from recent research, there are actually three types of lock-boxes for fat in the human body (white adipose tissue, brown adipose tissue, and tan adipose tissue).
The greatest challenge for the obesity doctor is getting into the fat lock-box. Some people’s boxes are like the “Jack-in-the-Box” you had as a child – just add a little exercise spinning the handle and the box pops open (These are those people that say, “Oh, just eat less and exercise and you’ll lose weight.”) For the majority of the people I see, it’s more like the lock above with a four or five part key required to turn the gears just right. (And, that key often only seems available on a quarter moon at midnight when the temperature is 72 degrees.) Fat cells, called adipocytes, require four, and possibly more, keys to open them up and access the fuel inside. Exercise is only one of those keys. However, exercise alone often fails.
Over the last 18 months, I have been surprisingly impressed with the results patients have by the addition of both medium chain triglycerides and exogenous ketones. A number of people have asked me, “Why do you encourage the addition of exogenous ketones to a person already following a ketogenic diet?”
Others just accuse me of self promotion, saying, “You’re just trying to sell a product!”
Or they exclaim, “Giving more ketones is just a waste of time and money.”
A few of the uneducated holler from across cyberspace, “You’re just going to cause ketoacidosis!”
Believe me, I’ve heard it all. And, the skepticism is understandable. I work with people every day, looking closely at weight gain/loss, metabolism, cholesterol, blood pressure, inflammation, etc. With any “low-carb” or “ketogenic product,” I test it out on myself and my family, before I offer it to my patients or even consider encouraging its use in my practice. I have this desire to understand “the how” and “the why” before I prescribe the who and when.
The Fat Lock-Box Keys
First , let’s talk about the adipocyte as a fat lock-box – and where you find the keys. Then, we’ll discuss how products may or may not help.
Insulin
There is only one door INTO the adipocyte for the fat, and the key to that door is insulin. Insulin stimulates an enzyme called lipoprotein lipase that essentially pulls the fat from the cholesterol molecule into the fat cell. Without insulin, fat doesn’t enter the fat cell. As a result, type I diabetics (those that make absolutely no insulin) look anorexic if they don’t take their needed insulin. Insulin is also the first key to the back door on the adipocyte. Actually, if there is too much insulin in the system, fat enters easily through the front door but cannot exit the back door (Picture 1). Insulin seals up the back door so that fat cannot exit very effectively.
That’s why insulin is the master hormone when it comes to obesity. You’ve got to lower the over-all insulin load to get the adipocyte slowing fat entry and increasing fat exit. If you don’t do that, I don’t care how much you exercise, 85% of the population will struggle with weight loss. Hmmm, seems kind a familiar to the last 50 years of our obesity epidemic, No?
Catecholamines
The second key to the back door of the fat cells are the catecholamines. These are adrenaline (epinephrine), norepinephrine, adrenocorticotropic hormone (ACTH) and even serotonin. These hormones are produced in the adrenal glands through exercise, fear and even recollection of powerful memories. Medications can also stimulate production of these hormones. The catecholamines stimulate cAMP. cAMP opens the fat cell, releasing fatty acids for fuel.
The thyroid hormone conversion of T4 to T3 also plays a role in uptake of the catecholamines by adnylyl cyclase (AC). Low levels of T3 (like those seen in hypothyroidism or in cases of thyroiditis) also inhibit unlocking of the fat lock-box. Conversion of T4 to T3 is driven by the presence of bile salts in the gut. Increase fat intake increases the presence of the bile salts which naturally leads to better T3 conversion. Hence my constant references to eating more fat and bacon. .
Inflammation & Medications
The third key is an inhibitory effect on adenylyl cyclase (AC) activity by alpha and beta adrenoreceptors, adenosine, prostaglandins, neuropeptide Y, peptide YY, HM74-R & nicotinic acid. These inhibitory and inflammatory hormones produced in the brain, gut and other areas decrease cAMP activity in the fat cell and slow fat loss. The fancy long names are all hormones causing inflammation. Of note, many are also stimulated by medications including blood pressure lowering drugs. Check with your doctor if the medications you are taking may be causing weight gain, or halting your weight loss.
Please note that the first three keys have effect on the cAMP pathway for release of fat from the adipocyte. These three keys turn on or off effective function of cAMP leading release of fatty acids from the fat cell.
Naturitic Peptides
The fourth key follows a separate pathway. This is why I’ve clinically seen patients experience weight loss even in the presence of higher insulin, inflammatory disease or hypothyroidism. This key activates release of the naturitic peptides (ANP, BNP). These hormones are released from the heart when it squeezes more powerfully. As the cardiac muscle contracts, it releases ANP & BNP hormones. These hormones stimulate the cGMP pathway in the adipocyte. It then activates hormone sensitive lipase (HSL) and perilipin to release free fatty acids. Again, this pathway is separate from the pathway by which the first three keys released fat. Exercise increases heart contractility, but is inhibited by high insulin levels. However, ketones themselves also stimulate this increased contractile effect.
Hypothalamus-Pituitary-Gonadal (HPG) Axis & Testosterone
There actually is a fifth key not referenced above. The fifth key to the fat lock-box amplifies testosterone’s presence through the HPG axis. Insulin resistance and leptin resistance lower testosterone in men and raise it in women, causing poly-cystic ovarian syndrome (PCOS). Normalizing insulin levels (with a ketogenic diet) while at the same time increasing ketones as the primary fuel powerfully resets the HPG axis through a complex series of hormonal reactions. Growth hormone is balanced and testosterone returns to a normal range.
Clinically, 60% of the people I see in the office have abnormal testosterone due to insulin resistance. This leads to hypogonadism in men and PCOS (abnormal periods, facial hair growth and/or infertility) in women. Restricting carbohydrates and maintaining nutritional ketosis by diet and/or addition of exogenous ketones has a powerful corrective factor in these people.
Testosterone influences the up-regulation of the alpha & beta adrenergic receptors (the 2nd & 3rd key above). Hence, if your testosterone is low, it has a suppression on the way that the catecholamines influence fatty acid release from the fat cells. If your testosterone and growth hormone are normal, muscle development and adrenaline stimulus from exercise helps amplify the use and mobilization of fat from the fat cell. In people with insulin resistance and leptin resistance, exercise and the catecholamines don’t have the same fat burning effect.
What Does This Actually Mean?
Yes, I have greatly simplified a series of very complex hormonal pathways in the explanation of the keys above. Why do you think understanding obesity has been so difficult? Think of your adipocytes as a fat lock-box.
What’s even more important is the knowledge that the fat cell DOES NOT open or close because of calories. There is no dogmatic calorie-meter on the wall of the fat cell. There is no calorie key to the fat lock-box. Really, . . . in the 50 years of studying fat, researchers haven’t found one. (Prove me wrong when you show me an electron micro-graph of a calorie-meter in the wall of a cell). Science has demonstrated multiple times that the lack of food from starvation or excessive fasting suppresses thyroid function (an inhibitory effect on key #3). Restricting calories actually inhibits fat loss in many people.
The fat lock-box keys I refer to above are hormone responses to the presence of macro-nutrients (food). That means, first reduce your carbohydrate intake by eating real food from good sources. You can learn how to get started by registering for my FREE six part weight loss mini-course. Second, be as active as you can. Third, reduce stress and medications that have inhibitory effect on catacholamines. Fourth, balance your thyroid. And, fifth, get into ketosis and consider adding exogenous ketones to your dietary regimen. It really is that simple.
References
(For those of you that still believe there is a calorie key – or just need something to do while in the bathroom):
- Lafontan et al. Arterioscler Thromb Vasc Biol. 2005
- Lenard NR, Obesity, 2008
- Li XF et al, Endo (April 2004) Vol 145
- Liu YY& Brent GA, Trends Endocrinol Metab. 2010 Mar; 21(3): 166–173
- Max Lafontan et al. Arterioscler Thromb Vasc Biol. 2005;25:2032-2042
- Skorupskaite K et al, Hum Rep Update, Mar 2014, vol 20
Coconut Oil – Duct Tape for the Broken Metabolism
Coconut oil can be found in just about every grocery store, health food store and coffee shop near you. It was made popular in the last few years by the highly advertised Bullet Proof Coffee claims of health and taste over the last few years. But in the last few days, the news outlets through video and print have made it clear that the American Heart Association (AHA) isn’t happy with our use of this “duct tape for one’s metabolism.” The AHA has long been a proponent of education against activities increasing the risk of heart disease. Since 1961 the AHA has decried the use of saturated fat, based on their support of Ansel Key’s diet heart hypothesis, and leading to over 60 years of preaching against the use of saturated fats from the pulpits of science. The claim is that 85% of coconut oil is saturated fat (this is the fat deemed “evil” by those “disciples of the low-fat cloth”). Yes, coconut oil is predominantly a saturated fat. And approximately 75% of that is medium chain triglycerides, the form that converts most efficiently into ketones, for those of us using ketogenic nutritional approaches to health. But is coconut oil really bad for your heart health?
Those of us using ketogenic diets know that LDL-C will commonly rise with increased saturated fat intake. And, we’ve know this for over twenty years. This is to be expected, because LDL-C is really comprised of three different LDL sub-particles (big fluffy, medium, and small dense). We’ve known for the last twenty years that increased saturated fat actually causes a shift in these particles to bigger “fluffier” particles. We also know that it’s the small dense LDL particles are the atherogenic/inflammatory particles participating in the formation of vascular disease (arterial blockage) and their presence in the blood is directly correlated with the level of triglyceride, and that the big “fluffy” particles actually reduce the risk of vascular disease. Those of us following ketogenic lifestyles and treating disease with these protocols also know that triglycerides levels are increased directly by increasing levels of insulin.
The 2015 British Medical Journal published a study reviewing the relevant 19 peer reviewed medical articles that included over 68,000 participants. This review showed that there is no association of high LDL-C (a calculated value of all the LDL sub-particles) with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart disease). In stark contrast to this landmark review, The American Heart Association’s Presidential Advisory published this week in the June 20, 2017 issue of Circulation states that saturated fat is the cause of increased LDL-C and elevated LDL-C is associated with an increase in death by cardiovascular disease. This boldfaced claim is based on a single small 4 year (2009-2013) literature review completed by the World Health Organization with a whopping 2353 participants, most of these studies only lasting 3-5 weeks (not nearly long enough to see fully effective cholesterol changes) and none of which had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement. From this singular study, the AHA concludes that elevated LDL-C is an indicator of increased cardiovascular mortality. That’s the equivalent of saying, “you know cars drive on the roads and cause pot holes, so we should all STOP driving cars because it is causing our freeway system to have increased pot holes.”
You can’t extrapolate mortality risk based on a single small study that doesn’t actually identify correlation or causation. But the AHA did exactly that in 1961, and they are trying to do it again today. The MR-FIT study, largest study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol. In fact, the Director of the study, Dr. William Castelli actually stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”
“We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active,” he said.
Isn’t that interesting?
So, is coconut oil, or any other food high in saturated fat to blame? Absolutely not! There is no solid evidence to support these facts and there hasn’t been in over 65 years. In fact, clinically, I find that the addition of coconut oil lowers triglycerides, decreases appetite, improves energy, improves skin tone, and plays a huge role in shifting the Omega 3/6 ratios to a more normal 2:1 level.
[clickToTweet tweet=”Is coconut oil, or any other food high in saturated fat to blame? Absolutely not! #docmuscles” quote=”Is coconut oil, or any other food high in saturated fat to blame? Absolutely not! There is no solid evidence to support these facts and there hasn’t been in over 65 years. #docmuscles”]
So, how does coconut oil help the broken metabolism? The majority of people I see in my office have insulin resistance to some degree. Insulin resistance is an over production of insulin in response to any form of carbohydrate or starch. Increasing your saturated fat, does two things. It provides a fantastic form of fuel, one your body can use very easily. And second, it will decrease your craving for starches and carbohydrates, naturally decreasing production of insulin and helping to improve insulin resistance over time.
If you want to learn more about using fat and improving insulin resistance, see my previous blog post here.
You can learn more about how our acceptance of bad science has lead to an obesity and diabetes epidemic in our country over the last 65 years by reading these books below:
But I Said You're The Good Kind of Fat…
Can Healthy Fats Make You Fat?
Are Zero-Carb Diets OK?
And, Can You Heal A Damaged Metabolism With Keto?
Listen in to KetoTalk.com for Podcast #26.
The health podcast legend, Jimmy Moore, and I talk about how much fat is too much. Or, is it? What’s the deal with Zero-carb ketogenic diets? We answer your questions and try to give you the most up-to-date knowlege regarding the ketogenic lifestyle and how it affects your metabolism. We zero in exclusively on all the questions people have about how being in a state of nutritional ketosis and the effects it has on your health.
There are a lot of myths about “keto” floating around out there and we shoot them down one at a time.
You can down-load it for free on iTunes or listen to KetoTalk.com on your computer.
Enjoy!!
Ketogenic Diet Halts Tumor Growth
It has long been understood that tumor cells of any kind require high levels of glucose to grow and spread (1,2). It is also recognized that higher levels of insulin, commonly found in patients with insulin resistance or type II diabetes, are 2.4 times more likely to stimulate the development of breast cancer (3). A diet low in glucose has thereby been theorized to be an adjunct to cancer treatment.
Ketogenic diets have been demonstrated to be therapeutically useful in the treatments of epilepsy and cardiovascular disease (4). A ketogenic diet is one in which carbohydrate levels are kept below 50 grams per day and fat intake is increased to the point that the body shifts its metabolism to use triglycerides, and the ketones derived from triglycerides, as the primary fuel source for the majority of the cells within the body. With this understanding in mind, the application of a ketogenic diet, one high in fat and protein with limited carbohydrate or glucose has been suggested as a adjunct to cancer treatments (5).
A recent study (6) in the Oncology Letters evaluated the benefits of a ketogenic diet in 78 cancer patients in clinical practice. A novel marker measuring the tumor cells use of glucose called transketolase-like-1 (TKTL1) was closely monitored, as was each of the 78 patients adherence to a ketogenic diet. Increased TKTL1 was noted in more aggressively active and growing tumors (7,8).
Among the 43 males and 35 females, 7 patients agree to and followed a fully ketogenic diet and 6 of them followed a partially ketogenic diet. Ketogenic meals were provided by a German company called Tavarlin that would prepare and mail ketogenic meals including oil, fat, snacks, bread, protein and energy drinks. Dietary journals were reviewed every three months over a period of about 10 months.
40 % of these patients experienced a halting of the tumor progression and 60% experienced improvement noted by normalization of TKTL1 or reduction in TKTL1, respectively. Those on a ketogenic diet demonstrated an average reduction of TKTL1 by approximately 50%.
This is the first study of its kind and has significant potential. Could dietary carbohydrate restriction be an effective cancer treatment or adjunct to cancer treatment?
Because the food diaries were based on reporting only, the sample study was very small, and patients treated in the outpatient setting have the possibility of variability in the standard oncologic treatments, the results must be interpreted with caution. However, the data is very promising. This study is one in which I have great interest as I have seen similar results in my clinic on a case by case basis.
Based on the limitations noted above, rigorous randomized control studies are needed, but this is an exciting an promising first step. Additionally, the presence of a marker for tumor growth that correlates with diet is remarkable. And, it provides the ketogenic specialist a possible measurement tool that could be used clinically.
References:
- Klement RJ and Kämmerer U: Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond) 8: 75, 2011
- Vaughn AE and Deshmukh M: Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrome c. Nat Cell Biol 10: 1477-1483, 2008.
- Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, Li J, Ho GY, Xue X, Anderson GL, et al: Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 101: 48-60, 2009.
- Paoli A, Rubini A, Volek JS and GrimaldiKA: Beyond weight loss: A review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr 67: 789-796, 2013.
- Ruskin DN and Masino SA: The nervous system and metabolic dysregulation: Emerging evidence converges on ketogenic diet therapy. Front Neurosci 6: 33, 2012.
- Jansen, N., Walach, H.”The development of tumours under a ketogenic diet in association with the novel tumour marker TKTL1: A case series in general practice”. Oncology Letters 11.1 (2016): 584-592.
- . Schwaab J, Horisberger K, Ströbel P, Bohn B, Gencer D, Kähler G, Kienle P, Post S, Wenz F, Hofmann WK, et al: Expression of Transketolase like gene 1 (TKTL1) predicts disease-free survival in patients with locally advanced rectal cancer receiving neoadjuvant chemoradiotherapy. BMC Cancer 11: 363, 2011.
- Zhang S, Yang JH, Guo CK and Cai PC: Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells. Cancer Lett 253: 108-114, 2007
Thinking Outside of the Box
The image above has nine dots within a square. Your task, using only four lines is to connect ALL nine dots WITHOUT ever raising your pen, pencil or finger (Please don’t use a sharpie on your computer screen . . . it doesn’t come off).
You may have seen this puzzle previously . . . it’s made its rounds in corporate training circles. But the underlying principle remains true. The solution requires you to expand your thinking or to “think outside the box.”
Whenever you find yourself on the side of the majority, it is time to pause and reflect. (Mark Twain)
Why should we limit ourselves to thinking outside the box. Can’t we just get rid of the box?
True discovery consists in seeing what everyone has seen . . . then, thinking what no one has thought.
The answer can be found when those four lines are used beyond the box our mind creates:
What good has the box done us? People were burned at the stake because they refused to believe the Earth was not the center of the universe. People were beheaded because they had a sneaking suspicion that the world was not flat.
Why is it so very hard to accept that our weight gain and diabetes are driven by a hormonal signal, and not by gluttony or caloric intake of fat? The definition of insanity is doing the same thing repetitively and expecting a different outcome. How long have you been restricting calories and fat with only minimal or no improvement in your weight, blood sugar, cholesterol or general feeling of health?
The main problem with the current thought model, or dogma, on the obesity’s cause is that it does not account for metabolic syndrome. Metabolic syndrome is insulin resistance. It is an over production of insulin in the presence of ANY form of carbohydrate (sugar or starch).
In the practice of medicine over the last 15 years, I noticed that a very interesting pattern emerged. There was always a spike in fasting and postprandial insulin levels 5-10 years prior to the first abnormal fasting and postprandial blood sugars. These patients were exercising regularly and eating a diet low in fat. But they saw continued weight gain and progressed down the path of metabolic syndrome. 10-15 years later, they fall into the classification of type II diabetes. What I now lovingly refer to as stage IV insulin resistance.
The only thing that seems to halt this progressive process with any degree of success is carbohydrate restriction. Fasting insulin levels return to normal, weight falls off, and the diseases of civilizations seem to disappear as insidiously as they arose.
So you tell me, is the world flat? Is the Earth the center of the universe?
What is a low carbohydrate or ketogenic diet? 15 years of practical in the trenches experience have helped me develop a very simple program to help you lose and maintain your weight. Access to this program, video help and access to blog articles at your fingertips are offered through my online membership site.
You can also hear me each week a I discuss low carbohydrate, paleolithic and ketogenic diets with the Legendary Jimmy Moore on KetoTalk.com
Caffeine . . . Weight Loss Wonder Boy or Sneaky Scoundrel?
I’ve been looking for the answer for quite some time. . . what role does caffeine play in your and my weight management journey? The answer gave me a headache. . . literally and figuratively.
As many of you, including my office staff, know, I love my Diet Dr. Pepper (and my bacon). I found that being able to sip on a little soda throughout the day significantly helped the carbohydrate cravings and munchies during a busy and stressful day at the office. Diet Dr. Pepper contains caffeine, however, I wasn’t really worried. Caffeine has been well know to have a thermogenic effect which increases your metabolism and has been thought for many years to help with weight loss among the weight loss community.
Diet Dr. Pepper is, also, one of only four diet sodas on the grocery store shelves that doesn’t contain acesulfame potassium (click here to see why most artificial sweeteners cause weight gain). The four diet sodas that I have been comfortable with my patients using are Diet Dr. Pepper, Diet Coke, Diet Mug Root-beer and Diet A&W Cream Soda. These are the last four hold out diet sodas that still use NutraSweet (aspartame) as the sweetener. Most of the soda companies have switched the sweetener in their diet sodas to the insulinogenic acesulfame potassium because it tastes more natural and aspartame has been given a media black eye of late. However, NutraSweet (aspartame) is the only sweetener that doesn’t spike your insulin or raise blood sugar (click here to find out why that is important).
Yes, I know. The ingestion of 600 times the approved amount of aspartame causes blindness in lab rats (but we’re not lab rats, and . . . have you ever met someone that drinks 600 Diet Dr. Peppers in a day? The lethal dose of bananas, which are high in potassium that will stop your heart, is 400). Aspartame can also exacerbate headaches in some (about 5% of people) and I’ve had a few patients with amplified fibromyalgia symptoms when they use aspartame. But for most of us, its a useful sweetener that doesn’t spike your insulin response, halting or causing weight gain.
But, over the last few years, I’ve noticed that increased amounts of Diet Dr. Pepper & Diet Coke seem to cause plateauing of weight and decreasing the ability to shift into ketosis, especially mine. I’ve also noticed (in my personal n=1 experimentation) that my ability to fast after using caffeine regularly seems to be less tolerable, causing headaches and fatigue 8-10 hours into the fast, symptoms that don’t seem to let up until eating. Through the process of elimination, caffeine seems to be the culprit.
After mulling through the last 10 years of caffeine research, most of which were small studies, had mixed results, used coffee as the caffeine delivery system (coffee has over 50 trace minerals that has the potential to skew the results based on the brand) and never seemed to ask the right questions, the ink from a study in the August 2004 Diabetes Care Journal screamed for my attention.
It appears that caffeine actually stimulates a glucose and insulin response through a secondary mechanism. The insulin surge and glucose response is dramatically amplified in patients who are insulin resistant. Caffeine doesn’t effect glucose or insulin if taken while fasting; however, when taken with a meal, glucose responses are 21% higher than normal, and insulin responses are 48% higher in the insulin resistant patient. Caffeine seems to only effect the postprandial (2 hours after a meal) glucose and insulin levels. The literature shows mixed responses in patients when caffeine is in coffee or tea, probably due to the effect of other organic compounds (1).
Caffeine also diminishes insulin sensitivity and impairs glucose tolerance in normal and already insulin resistant and/or obese patients. This is seen most prominently in patients with diabetes mellitus type II (stage IV insulin resistance). Caffeine causes alterations in glucose homeostasis by decreasing glucose uptake into skeletal muscle, thereby causing elevations in blood glucose concentration and causing an insulin release (2-6).
Studies show that caffeine causes a five fold increase in epinephrine and a smaller, but significant, norepinephrine release. The diminished insulin sensitivity and exaggerated insulin response appears to be mediated by a catacholamine (epinephrine, norepinephrine & dopamine) induced stress response (5). Caffeine has a half life of about 6 hours, that means the caffeine in your system could cause a catacholamine response for up to 72 hours depending upon the amount of caffeine you ingest (7).
The reason for my, and other patient’s, headaches and fatigue after a short fast was due to the exaggerated stress hormone response. Increased levels of insulin were induced by a catacholamine cascade after caffeine ingestion with a meal, dramatically more amplified in a person like me with insulin resistance. The caffeine with the last meal cause hypoglycemia 5-7 hours into the fasting, leading to headaches and fatigue that are only alleviated by eating.
Even when not fasting, the caffeine induced catacholamine cascade causes up to 48% more insulin release with a meal, halting weight loss and in some cases, causing weight gain.
Caffeine is not the “Wonder-Boy” we thought it was.
How much caffeine will cause these symptoms? 50 mg or more per day can have these effects.
Ingestion of caffeine has the following effects:
- 20-40 mg – increased mental clarity for 2-6 hours
- 50-100 mg – decreased mental clarity, confusion, catacholamine response
- 250-700 mg – anxiety, nervousness, hypertension & insomnia
- 500 mg – relaxation of internal anal sphincter tone (yes . . . you begin to soil yourself)
- 1000 mg – tachycardia, heart palpitations, insomnia, tinnitus, cognitive difficulty.
- 10,000 mg (10 grams) – lethal dose (Yes, 25 cups of Starbucks Coffee can kill you)
The equivalent of 100 mg of in a human was given to a spider, you can see the very interesting effect on productivity. How often does the productivity of the day feel like the image below?
Beware that caffeine is now being added to a number of skin care products including wrinkle creams and makeup. Yes, caffeine is absorbed through the skin, so check the ingredients on your skin care products.
Diet Dr. Pepper, my caffeine delivery system of choice, has slightly less caffeine (39 mg per 12 oz can or 3.25 mg per oz) than regular Dr. Pepper. I found myself drinking 2-3 liters of Diet Dr. Pepper per day (long 16-18 hour work days in the office). After doing my research, I realized that my caffeine tolerance had built up to quite a significant level (230-350 grams per day).
So, a few weeks ago, I quit . . . cold turkey.
Did I mention the 15 withdrawal symptoms of caffeine? (8)
- Headache – behind the eyes to the back of the head
- Sleepiness – can’t keep your eyes open kind of sleepiness
- Irritability – everyone around you thinks you’ve become a bear
- Lethargy – feels like your wearing a 70 lb lead vest
- Constipation – do I really need to explain this one?
- Depression – you may actually feel like giving up on life
- Muscle Pain, Stiffness, Cramping – feel like you were run over by a train
- Lack of Concentration – don’t plan on studying, doing your taxes or performing brain surgery during this period
- Flu Like Illness – sinus pressure and stuffiness that just won’t clear
- Insomnia – you feel sleepy, but you can’t sleep
- Nausea & Vomiting – You may loose your appetite
- Anxiety – amplified panic attacks or feeling like the sky is falling
- Brain Fog – can’t hold coherent thoughts or difficulty with common tasks
- Dizziness – your sense of equilibrium may be off
- Low Blood Pressure & Heart Palpitations – low pressure and abnormal heart rhythm
I experienced 13 of the 15 that lasted for 4 days. I do not recommend quitting cold turkey unless you have a week off and someone to hold your hand, cook your meals and dose your Tylenol or Motrin. My wife thought I was dying. . . I thought I was dying on day two. I actually had a nightmare about buying and getting into my own coffin. It can take up to three weeks to completely recover from caffeine withdrawal.
The other way to quit is to decrease your caffeine intake by 50 mg every two days. That means decrease caffeine by:
- 1 can of soda every two days
- 1/4 cup of coffee every day
- 1/2 can of Energy Drinks every two days
- 1 cup of tea every two days
The benefit of this method is that withdrawal symptoms are much less severe without the caffeine headache and the ability to remain productive. It will take longer, but quitting cold turkey is not a pretty picture. Been there . . . done that, . . . and I’m not going back. I actually lost another half inch off my waistline by day 5 of caffeine discontinuation.
What is the take home message here? If you have any degree of insulin resistance, caffeine makes it worse and will amplify your weight gain as well as decrease the productivity of your day.
References:
- Lane JD, Barkauskas CE Surwit RS, Feinglos MN, Caffeine Impairs Glucose Metabolism in Type II Diabetes, Diabetes Care August 2004 vol. 27 no. 8 2047-2048; doi:10.2337/diacare.27.8.204
- Jankelson OM, Beaser SB, Howard FM, Mayer J: Effect of coffee on glucose tolerance and circulating insulin in men with maturity-onset diabetes. Lancet 1: 527–529, 1967
- Graham TE, Sathasivam P, Rowland M, Marko N, Greer F, Battram D: Caffeine ingestion elevates plasma insulin response in humans during an oral glucose tolerance test. Can J Physiol Pharmacol 79:559–565, 2001
- Greer F, Hudson R, Ross R, Graham T: Caffeine ingestion decreases glucose disposal during a hyperinsulinemic-euglycemic clamp in sedentary humans.Diabetes 50:2349–2354, 2001
- Keijzers GB, De Galan BE, Tack CJ, Smits P: Caffeine can decrease insulin sensitivity in humans. Diabetes Care 25:364–369, 2002
- Petrie HJ, et al. Caffeine ingestion increases the insulin response to an oral-glucose-tolerance test in obese men before and after weight loss. American Society for Clinical Nutrition. 80:22-28, 2004
- Evans SM, Griffiths RR, Caffeine Withdrawal: A Parametric Analysis of Caffeine Dosing Conditions, JPET April 1, 1999 vol. 289no. 1 285-294
- Noever R, Cronise J, Relwani RA. Using spider-web patterns to determine toxicity. NASA Tech Briefs April 29,1995. 19(4):82. Published in New Scientist magazine, 29 April 1995
How Do You Know if You’re Insulin Resistant?
How do you know if you're insulin resistant? What questions need to be asked? What should your numbers be? And, many other great ketosis questions. Also, why does Dr. Nally look like he has dirt on his chin? See it here . . .
The 5 Myths of Weight Loss
This evening we covered the 5 myths of weight loss identified through the National Weight Control Registry’s research findings. What causes “wrinkle face” for Dr. Nally? We also talked about & answered 20 minutes of rapid fire questions ranging from the amount of protein you need daily to the likelihood a human could be a bomb calorimeter . . . exciting stuff!!
You can watch the video stream below. Or you can Katch the replay with the rapid stream of exciting comments here at Katch.me/docmuscles.
Diabetes Mellitus – Really the Fourth Stage of Insulin Resistance
I just completed my reading of Dr. Joseph Kraft’s Diabetes Epidemic & You. This text originally printed in 2008 and was re-published in 2011. I am not really sure why I have never seen this book until now, but I could not put it down. I know, I am a real life medical geek. But seriously, you should only read this book if you are concerned about your health in the future. Otherwise, don’t read it.
For the first time in 15 years, someone has published and validated what I have been seeing clinically in my office throughout my career. Dr. Kraft is a pathologist that began measuring both glucose and insulin levels through a three hour glucose tolerance blood test at the University of Illinois, St. Joseph Hospital in Chicago. This test consists of checking blood sugar and insulin in a fasted state, and then drinking a 100 gram glucose load followed by checking blood sugar and insulin at the 30, 60, 120 and 180 minute marks (a total of three hours).
Dr. Kraft completed and recorded this test over a period of almost 30 years on 14,384 patients between 1972 and 1998. His findings are landmark and both confirm and clarify the results that I have seen and suspected for years.
I am convinced that our problem with treating obesity, diabetes and the diseases of civilization has been that we defined diabetes as a “disease” based on a lab value and a threshold instead of identifying the underlying disease process. We have been treating the symptoms of the late stage of a disease that started 15 to 20 years before it is ever actually diagnosed. Diabetes is defined as two fasting BS >126, any random blood sugar >200, or a HbA1c >6.5%. (Interestingly this “disease” has been a moving target. When I graduated from medical school it was two fasting blood sugars >140 and the test called hemoglobin A1c (HbA1c) that we use today for diagnosis didn’t even exist). The semantics associated with this problem is that many of us recognize that the disease is not actually diabetes. The disease is (as far as we understand it today) insulin resistance or hyperinsulinemia. This is where Dr. Kraft’s data is so useful. Diabetes, as it is defined above, is really the fourth stage of insulin resistance progression over a 15-20 year period and Dr. Kraft’s data presents enormous and very clear evidence to that effect.
When I first entered private practice 15 years ago, I noticed a correlation and a very scary trend that patients would present with symptoms including elevated triglycerides, elevated fasting blood sugar, neuropathy, microalbuminuria, gout, kidney stones, polycystic ovarian disease, coronary artery disease and hypertension that were frequently associated with diabetes 5-15 years before I ever made the diagnosis of diabetes mellitus. I began doing 2 hour glucose tolerance tests with insulin levels and was shocked to find that 80-85% of those people were actually diabetic or very near diabetic in their numbers. The problem with a 2 hour glucose tolerance test, is that if you are diabetic or pre-diabetic, you feel miserable due to the very profound insulin spike that occurs. A few patients actually got quite upset with me for ordering the test, both because of how they felt after the test, and the fact that I was the only physician in town ordering it. So, in an attempt to find an easier way, I found that the use of fasting insulin > 5 nU/dl, triglycerides > 100 mg/dl and small dense LDL particle number > 500 correlated quite closely clinically with those patients that had positive glucose tolerance tests in my office. There is absolutely no data in the literature about the use of this triangulation, but I found it to be consistent clinically.
I was ecstatic to see that Dr. Kraft plowed through 30 years and over 14,000 patients with an unpleasant glucose tolerance test and provided the data that many of us have had to clinically triangulate. (I’m a conservative straight white male, but if Dr. Kraft would have been sitting next to me when I finished the book this afternoon, I was so excited that I probably would have kissed him.)
Insulin resistance or hyperinsulinemia (the over production of insulin between 2-10 times the normal amount after eating carbohydrates) is defined as a “syndrome” not a disease. What Dr. Kraft points out so clearly is that huge spikes in insulin occur at 1-2 hours after ingestion of carbohydrates 15-20 years prior to blood sugar levels falling into the “diabetic range.” He also demonstrates, consistently, the pattern that occurs in the normal non-insulin resistant patient and in each stage of insulin resistance progression.
The information extrapolated from Dr. Kraft’s research give the following stages:
From the table above, you can see that the current definition of diabetes is actually the fourth and most prolifically damaging stage of diabetes. From the data gathered in Dr. Kraft’s population, it is apparent that hyperinsulinemia (insulin resistance) is really the underlying disease and that diabetes mellitus type II should be based upon an insulin assay instead of an arbitrary blood sugar number. This would allow us to catch and treat diabetes 10-15 years prior to it’s becoming a problem. In looking at the percentages of these 14,384 patient, Dr. Kraft’s data also implies that 50-85% of people in the US are hyperinsuliemic, or have diabetes mellitus “in-situ” (1). This means that up to 85% of the population in the U.S. is in the early stages of diabetes and is the reason 2050 projections state that 1 in 3 Americans will be diabetic by 2050 (2).
Insulin resistance is a genetically inherited syndrome, and as demonstrated by the data above has a pattern to its progression. It is my professional opinion that this “syndrome” was, and actually is, the protective genetic mechanism that protected groups of people and kept them alive during famine or harsh winter when no other method of food preservation was available. It is most likely what kept the Pima Indians of Arizona, and other similar groups, alive while living for hundreds of years in the arid desert. This syndrome didn’t become an issue among these populations until we introduced them to Bisquick and Beer.
The very fascinating and notably exciting aspect of this whole issue is that insulin resistance is made worse by diet and it is completely treatable with diet. This is where the low carbohydrate diet, and even more effective ketogenic diet or lifestyle becomes the powerful tool available. Simple carbohydrate restriction reverses the insulin spiking and response. In fact, I witness clinical improvement in the insulin resistance in patients in my office over 18-24 months every day. You can get a copy of my Ketogenic Diet here in addition to video based low carbohydrate dietary instruction.
Until we are all on the same page and acknowledge that diabetes is really the fourth stage of progression on the insulin resistance slippery slope, confusion and arguments about treatment approaches will continue to be ineffective in reducing the diseases of civilization.
References:
- Kraft, JR. Diabetes Epidemic & You: Should Everyone Be Tested? Trafford Publishing, 2008, 2011. p 1-124
- Boyle JP et al. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence, http://www.pophealthmetrics.com/content/8/1/29 Accessed November 22, 2015
The Ketogenic Antidote to Chronic Renal Disease
It is well know that one of the most profound complications of diabetes is damage to the kidney and the very small arteries within the kidney acting as your body’s filtration system. The kidney begins to lose the ability to adequately filter and retain microscopic protein progressively over time. As the blood sugar and insulin levels continually rise over time in the patient with diabetes or pre-diabetes, damage to the delicate filtering system of the kidneys occur. This very common and progressively damaging problem is called “nephropathy.”
We knew in 1972 that patients with diabetes had thickening of the basement membrane or endothelium of the small tubles within the kidneys. In fact, 98.6% of diabetics tested had thickening of this area of endothelium and tubules also called the renal glomeruli (1). This allows the glomerulus or filtration system of the kidney to become more “leaky” and microscopic protein loss begins to occur through the kidney. This loss of important proteins in the blood is called “albuminuria” or “micro-albuminuria.” It is a flag that further damage of the kidney can and will occur without making significant changes to lower the blood sugar and the insulin. As of today, it is not totally clear how the basement membrane is damaged at the microscopic level, however, there is some evidence that elevated insulin has both a physical and immune type effect that stimulates oxidative stress, atherogenesis, immunoglobulins, as well as the formation advanced glycation end products leading to endothelial wall damage (2).
Recent research reveals that a ketogenic diet effectively repairs and/or completely reverses the albuminuria (3).
Evidence in my office of the significant improvement in micro-albumin can be seen in the one of a number of case studies below:
72 year old male with history of diabetes, diabetic nephropathy already treated with full dose statins, ACE inhibtors, metformin, and Januvia. (Remember, microalbumin should be <30 mg/g)
Date Microalbumin HbA1c
8/12/2010 2264 mg/g 6.4% Started carb restriction <30 g per day.
10/01/2010 1274 mg/g 5.2%
1/08/2011 1198 5.8% Admits to cheating over holidays
12/26/2013 2434 mg/g 6.8% Returned from 2 yr travel-off diet
2/27/2014 399 mg/g 6.3% Restarted carb restriction <20g per day
6/20/2014 190 mg/g 7.0% Traveling – no carb restriction
10/31/2014 280 mg/g 6.9% Partial carb restriction <10 g/meal
3/14/2015 97 mg/g 6.8%
The patient began following a ketogenic diet in 2010. After improvement he moved out of town for two years and “fell of the wagon.” Upon returning h restarted his carbohydrate diet and was only partially following it. As you can see, he also admitted to some cheating on the carbohydrate restriction over the holidays. In light of this, carbohydrate restriction decreased his albuminuria from 2400 to 97 mg/g within a period of 18 months.
References:
- Siperstein MS, Unger RH, Madison LL. “Further Electron Microscopic Studies of Diabetic Microagniopathy.” Early Diabetes: Advances in Metabolic Disorders, sup 1. New York: Academic Press, 1972, p261-271.
-
Nasr SH, D’Agati VD. “Nodular glomerulosclerosis in the nondiabetic smoker.” J Am Soc Nephrol. 2007;18(7):2032.
- Poplawski MM, Mastaitis JW, Isoda F, Grosjean F, Zheng F, Mobbs CV (2011) Reversal of Diabetic Nephropathy by a Ketogenic Diet. PLoS ONE 6(4): e18604. doi:10.1371/journal.pone.0018604
How to Stay Motivated on Carbohydrate Restriction
This evening on PeriScope, we talked about the 10 things you can do to stay motivated on your low-carb lifestyle. A number of great questions were asked including:
- How much carbohydrate should be restricted?
- What labs should you be monitoring regularly?
- What’s a normal blood sugar?
- Why is Dr. Nally freezing in Denver?
- Is fermented food good for you?
- Why should you eat pickles and kimchi even when you’re not pregnant?
And, much much more . . . It’s like a college ketogenic course on overdrive . . . for FREE!!!
You can see the PeriScope with the comments rolling in real-time here: katch.me/docmuscles
Or, you can watch the video stream below:
See you next time.
How Fat Makes You Skinny . . . (Eating Fat Lowers Your Cholesterol?!)
Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.
First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)
However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).
There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).
Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.
Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.
Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).
Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.
I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:
https://www.katch.me/docmuscles/v/2f0b6d07-d56a-368b-b4f6-34a5ab3da916
Or, you can watch the video below:
References:
- Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
- Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
- Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
- Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
- Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
- Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
- Shai I et al. Cirulation. 2010; 121:1200-1208
- Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
- Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy
Reversal of Diabetes in the Ketogenic Zone – A Case Report
This week I had the pleasure of seeing a really nice 46 year old Hispanic male who is fairly new to the office. He came back in to see me in follow up on his diabetes. To give you a bit of background history, the patient came to see me about 6 months ago, just not feeling very well. Based on his symptoms of fatigue, history of elevated blood sugar and family history, lab work was completed.He saw us initially with a Hemoglobin A1c of 12.3% in June (normal should be 4.9%-5.6%). This means he had an average blood sugar over the previous three months of about 310 mg/dL (normal should be < 110 mg/dL).
Past Medical History include: Diabetes Mellitus – type II (not on any medications when initially seen), Hypertension (high blood pressure), Dyslipidemia (elevated cholesterol) and a non-specific heart arrhythmia.
Medications: None
Surgeries: Knee & shoulder arthroscopies
Family History: Father Diabetes, Stroke, Heart Disease, Hypertension, Elevated Cholesterol
Social History: Non-Smoker, Limited Alcohol Use
He related to me that he had been on metformin before, however, had some significant diarrhea and was not interested in using this medication EVER again. A previous doctor had tried Victoza© (liraglutide), a GLP-1 inhibitor, but he didn’t use it for very long as he didn’t really see much change with this medication.
After getting his labs back, we had a very long conversation about the need to either fix his diet dramatically, or he may be looking at using 3-4 oral medications or even insulin to control his blood sugar.
When I see average blood sugars (HbA1c) stay over 6.5% (or greater than 140 mg/dL), the risk for retinal, kidney and nerve damage is significant and often irreversible after 4-5 years. Most physican’s are affraid to lower the HbA1c to less than 7.0% with medications due to low blood sugar events, and so the diabetes community has “settled” with 7.0% as being effective. However, it still isn’t low enough. I saw this happen with my father and with other members of me family. I’ve seen it happen over and over with my patients over the last 15 years when they have not lowered their blood sugar and reduced the high insulin loads that occur in response to those high blood sugar levels. It has been my experience that HbA1c can be very safely lowered to the normal range, as low as 5.2-5.6% without symptomatic low blood sugars, with the correct diet and careful use of medications.
So, my patient, above, committed to change. I was worried that diet alone would not be able to lower these levels enough to be effective so we discussed tight carbohydrate restriction, the addition of methlyated folate and chromium and a re-trial of a low dose of Victoza© (liraglutide), which he had at home.
I didn’t see him for about three months. When he followed up this week I was amazed. I was amazed because I rarely see more than 1.5% drop in HbA1c with the addition of Victoza© (liraglutide). The additional 4.5% of drop with diet was dramatically impressive.
When we talked, he told me that all he has done differently is use the Victoza© (liraglutide) and cut his carbohydrate intake to less than 10 grams per meal (Yes, he did admit to occasionally cheating).
You can see the dramatic results:
June 2015 |
September 2015 |
|
Glucose |
258 |
103 |
HbA1c |
12.3% |
6.3% |
Urine Creatinine (Random) |
208 |
72 |
|
||
Total Cholesterol (mg/dL) |
219 |
218 |
Triglycerides (mg/dL) |
137 |
117 |
HDL-C (mg/dL) |
38 |
37 |
LDL-C (mg/dL) |
154 |
158 |
LDL-P (nmol/L) |
2172 |
1691 |
Small dense LDL-P (nmol/L) |
1289 |
419 |
|
||
TSH (mU/L) |
1.75 |
|
|
As you can see, a dramatic change in his blood sugar has occurred in a three month interval. Not only that, we see a significant change in his cholesterol profile.
Some might argue that this is the Victoza© (liraglutide) doing this. I can tell you, in the 15 years I’ve been doing this and in the 5 years that Victoza© (liraglutide) has been available in the U.S., I have never seen a drug reduce blood sugar or cholesterol this dramatically.
Previously, we looked at LDL-C for heart disease risk, however, I have multiple patients that have had heart disease with normal LDL-C ( <100 mg/dL). LDL-C is just a summation of all the particles. The LDL particle is actually made up of three sub-types and it is specifically the small dense particle that causes the vascular risk. You can see a dramatic normalization of the small dense particle LDL with no change in LDL-C and minimal change in Total Cholesterol in the patient’s labs when he reduces his carbohydrate intake. This is a pattern I see every single day. When serial carotid ultrasound studies are completed, I see reduction in blockage and reduction in the vascular wall thickening. I will be very interested to see the vascular studies on this patient and I will await his results as he tightens up his diet even further.
All in all, he has dramatically brought his diabetes under control with carbohydrate restriction and if he continues this lifestyle, he has reduced his risk for retinal damage, reduced his risk for kidney damage, reduced his risk for nerve damage and essentially added 20 years to his life.
(Disclosures: Dr. Nally has no vested interest, monitary or otherwise, in Novo Nordisc or it’s products including liraglutide.)
The Dreaded Seven . . . (Seven Detrimental Things Caused by High Insulin Loads)
85% of the people that walk through my office doors have some degree of insulin resistance.
What is “insulin resistance?” It is an over production of insulin in response to ANY form of carbohydrate intake (yes, even the “good carbs” cause an insulin over-response in a person with insulin resistance.)
How do I know this? Because I routinely check insulin levels (I check them every three months) and the down stream markers of insulin on a large number of the patients that I see. I have been fascinated by the fact that a diet high in both sugar and fat [like the Standard American Diet, (SAD) diet] turn on the genetics leading to insulin resistance. Starch and sugar load the genetic gun.
Insulin acts like a key at the glucose doorway of every cell in your body. In many people, the insulin signal is blocked by hormones produced in the fat cell and the the insulin, acting like a “dull or worn out key” – can’t open the glucose doorway as efficiently.
So, the body panics, and releases extra insulin in response to the same load of carbohydrate or glucose. People with insulin resistance will produce between 2-20 times the normal amount of insulin in response to a simple carbohydrate load. Recent studies(1, 2) reveal high cholesterol and diets high in both fat and carbohydrate cause insulin resistance to progress or worsen.
So, instead of producing enough insulin to accommodate the one slice of bread or the one apple that you might eat, the insulin resistant person produces enough insulin for an entire loaf of bread or an entire bushel of apples. This excess insulin then stimulates one or all of the following:
- Weight Gain – Insulin directly stimulates weight gain by activating lipoprotein lipase to take up triglycerides into the fat cells. This causes direct storage of fat and increases your waistline. (3)
- Elevated Triglycerides – Insulin directly stimulates production of free fatty acids and triglycerides through hepatic gluconeogenesis and is even more notably amplified by the broken signaling mechanism of the FOX-01 phosphorylation mechanism in patients with insulin resistance. (4)
- Increased number of Small Dense LDL (sdLDL) particles – Low density lipoprotein (LDL, or “bad cholesterol”) is actually comprised of various sized lipoproteins including small, medium and large. As triglycerides increase, the small dense LDL particle numbers increase. Research points to the fact that it is the small dense particle that is highly atherogenic (leading to the formation of vascular plaques within the arteries). (5, 8)
- Elevated Uric Acid – Leptin resistance and insulin resistance syndromes are often found together and are suspected to have significant influence on each other. High insulin loads lead to “sick adipose cells” causing leptin resistance. This has a dramatic effect on hepatic fructose metabolism increasing the production of uric acid. Excess insulin suppresses urinary excretion of uric acid and dramatically increases serum content of uric acid and the risk of kidney stones and gout. (6, 7)
- Increased Inflammation – Increased levels of circulating insulin have a direct correlation on raising many of the inflammatory markers and hormones including TNF-alpha and IL-6 in the body (9). Any disease process that is caused by chronic inflammation can be amplified by increased circulating levels of insulin including asthma, acne, eczema, psoriasis, arthritis, inflammatory bowel and celiac disease, etc.
- Elevated Blood Pressure – Increased uric acid production from insulin resistance as noted above directly suppresses production of nitric oxide within the vasculature and increases blood pressure (7). This completes the triad of metabolic syndrome (elevated triglycerides & cholesterol, weight gain, and elevated blood pressure) found in patients with insulin resistance.
- Water Retention – We have known for many years that insulin affects the way the kidney uses sodium in the distal nephron. Insulin has a direct effect on sodium retention in the kidney. As insulin levels rise, the kidney retains increased levels of sodium (10). Water follows sodium and thereby causes fluid retention. This is the reason that many of my insulin resistant patients who have struggled with leg swelling and edema suddenly improve when they correct their diet and their high circulating insulin levels fall. It is also the reason that many of my patients show up in my office after the holidays with swollen legs and amplified swelling in their varicose veins after cheating on their ketogenic diets.
If you are plagued by any or all of these, my first suggestion is to see your doctor and get screened for insulin resistance. I treat patients with these every day and have reversed these effects in thousands of patients with the correct diet and/or medications. Having seen these signs and patterns over the last 20 years of medical practice, I am still astonished every day by the dramatic effect our diet plays on the hormonal changes within the body. Remember that the food you eat is actually the most powerful form of medicine . . . and the slowest form of pernicious poison.
A ketogenic or carnivorous diet is your first step.
We take most insurances, however, check out my concierge program or my Direct Primary Care program if you are interested in an alternative to insurance.
References:
- Cholesterol Elevation Impairs Glucose-Stimulated Ca2+Signaling in Mouse Pancreatic β-Cells, Endocrinology, June 2011, Andy K. Lee, Valerie Yeung-Yam-Wah, Frederick W. Tse, and Amy Tse; DOI: http://dx.doi.org/10.1210/en.2011-0124
- Glucose-Stimulated Upregulation of GLUT2 Gene Is Mediated by Sterol Response Element–Binding Protein-1c in the Hepatocytes, DIABETES, VOL. 54, JUNE 2005; Seung-Soon Im, Seung-Youn Kang, So-Youn Kim, Ha-il Kim, Jae-Woo Kim, Kyung-Sup Kim and Yong-Ho Ahn
- Obesity and Insulin Resistance. J Clin Invest. 2000 Aug;106(4):473-81.Kahn BB, Flier JS
- Selective versus Total Insulin Resistance: A Pathogenic Paradox, Cell Metabolism, Volume 7, Issue 2, 6 February 2008, Pages 95–96, Michael S. Brown, Joseph L. Goldstein
- Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy, Gentile M, Panico S, et al., Clinica Chimica Acta, 2013
- Sugar, Uric Acid and the Etiology of Diabetes and Obesity. Diabetes. 2013;62(10):3307-3315, Richard J. Johnson; Takahiko Nakagawa; L. Gabriela Sanchez-Lozada; Mohamed Shafiu; Shikha Sundaram; Myphuong Le; Takuji Ishimoto; Yuri Y. Sautin; Miguel A. Lanaspa
- Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep;110(9):1307-21. doi: 10.1016/j.jada.2010.06.008. Lustig RH
- Cardiovascular Risk in Patients Achieving Low-Density Lipoprotein Cholesterol and Particle Targets. Atherosclerosis. Vol 235; 585-591, May 2014, Peter P. Toth, Michael Grabner, Rajeshwari S. Punekar, Ralph A. QuimboMark J. Cziraky c, Terry A. Jacobson
- Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome The Insulin Resistance Atherosclerosis Study (IRAS), Circulation, July 2000, 102:42-47; Andreas Festa, MD; Ralph D’Agostino, Jr, PhD; George Howard, DrPH; Leena Mykka¨nen, MD, PhD; Russell P. Tracy, PhD; Steven M. Haffner, MD
- The Effect of Insulin on Renal Sodium Metabolism. Diabetologia. September 1981, Volume 21, Issue 3, pp 165-171. R. A. DeFronzo
My Copy of The Ketogenic Cookbook Arrived!!!!
Look what I just got in the mail this afternoon. . . my copy of Jimmy Moore & Maria Emmerich’s The Ketogenic Cookbook!
Wow. Great info, fantastic recipes (with amazing pictures, by the way!) and the most up to date ketogenic advise out there. I’m impressed.
What a fantastic addition to my library. I was going snap a few shots of my favorite dishes in it, but my wife picked it up while I was typing and won’t put it down. . . .
Thanks, Jimmy Moore’s Livn’ La Vida Low-Carb & Maria’s Mind Body Health!!
Outside of the Box
Whenever you find yourself on the side of the majority, it is time to pause and reflect.
– Mark Twain
Why should we limit ourselves to thinking outside the box. Can’t we just get rid of the box?
True discovery consists in seeing what everyone has seen . . . then, thinking what no one has thought.
People were burned at the stake because they refused to believe the Earth was not the center of the universe. They were beheaded because they had a sneaking suspicion that the world was not flat.
Is it really that hard to accept that our weight gain and diabetes is driven by a hormonal signal, and not by gluttony or caloric intake of fat?
The challenge with the current thought model on the cause of obesity is that it does not account for metabolic syndrome. In the practice of medicine over the last 15 years, an interesting pattern has emerged. I noticed that there was a spike in fasting and postprandial insulin levels 5-10 years prior to the first abnormal fasting and postprandial blood sugars. These patients were exercising regularly and eating a diet low in fat. But they saw continued weight gain and progressed down the path of metabolic syndrome. 10-15 years later, they fall into the classification of type II diabetes.
The only thing that seems to halt this process in these patients is carbohydrate restriction. Fasting insulin levels return to normal, weight falls off, and the diseases of civilizations disappear as insidiously as they arose.
So you tell me, is the world flat? Is the Earth the center of the universe?
The Truth is . . . Caloric Restricted Exercise Won’t Work
This post isn’t going to win me any friends . . . in fact, mentioning this topic a few days ago has already angered a number of them and resulted in an online tongue lashing by a few others. However, I can’t resist. And, based on some very persuasive data and personal experience, I don’t care.
Truth is truth . . . it doesn’t change no matter how you spin it, or attempt to fit it into your paradigm. The problem is what we have accepted in the last 40-50 years as “the scientific truth about getting healthy” is far from truth. By getting healthy, I’m implying the application of main-stream methods accepted to lose weight, reduce cholesterol, improve blood pressure and reduce your risk of heart disease and diabetes.
For the last 40 years we’ve been told that the only way to get and live healthy is to restrict our calories. This main-streamed advise continues even today in our USDA 2010 Dietary Guidelines. And, if you ascribe to this futile dogma propagated since the 1970’s, then you’ll know that the “only acceptable way” to do this is to “eat less fat” (because fat is the most caloric dense of the macro-nutrients, right?) and to “exercise more” (because that’s how we burn calories, right?!) Well, that’s what I thought, too. And that is the health prescription I doled out to my-self and to all of my patients for the first 8 years of my practice.
Interestingly, most of them, including myself, took that prescription of a caloric restricted diet of 1200-1500 calories per day and exercise 3-6 days a week for 30-60 minutes and ran with it. Personally, I restricted calories to 1200-1500 per day and began running triathlons. I performed cardiac monitored running, swimming and cycling for an hour a day during the week and 2 hours on the weekend. I lifted weights 2-3 days per week as well. Guess what it got me? Fat.
It raised my triglycerides by 100 points, elevated my LDL-C and increased my waistline by 3 inches. Yes, I gained weight. But, hey, my doctor was happy because my HDL-C went up by 4 points.
I saw this identical pattern with 3/4ths the patients in my office. A fourth of my patient’s (the group without any genetic insulin resistance) saw weight loss and improvement in their cholesterol profiles, but the rest didn’t. I had the exciting opportunity to introduce the saddened and discouraged 3/4ths of my patients to STATIN drugs and blood pressure medications. My average patient’s gained 2-3% of their body fat each year. Those that exercised like fiends were lucky if their weigh gain just stabilized.
What I saw in my office over a period of eight years was that exercise and caloric restriction didn’t work. But I couldn’t say that, because that goes against everything your 8th grade health teacher taught you. It contradicted your neighborhood dietitian, and it spat in the face of the food pyramid and the USDA Guidelines. The Government wrong? Never. . . . Speaking contradictory of the calorie-in/calorie-out exercise dogma was heresy, right? Contradict, Dr. Ornish, wouldn’t be heard of?!!
If I’ve learned one thing in my medical career, it is this: “Don’t be afraid to question everything” – even Dr. Dean Ornish, the USDA and the American Heart Association. And, fascinatingly, I’m not the only on that did.
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Three Massive Studies did just that . . . question whether this exercise and caloric restriction dogma really works. This is what applying exercise and caloric cutting did for almost 67,000 people between 1972 and 2010 – little to nothing.
WHAT?!! Nothing?! You can’t be serous?
The first of these trials was the MRFIT (Multiple Risk Factor Intervention) Trial. It started in 1972, looking at 12,866 men with high risk for heart disease and followed them over seven years. All of them were placed on caloric restricted low fat diets and encouraged to exercise. It demonstrated that low fat diets and exercise FAILED to reduce weight or stop coronary artery disease in 100% of the cases. Don’t believe me? Read it for yourself (JAMA. 1982; 248 (12):1465-1477).
The second of these trials was the Women’s Health Initiative (WHI). This study started in 1991 and followed 48,835 women (yes, that’s a small city of women) for eight years. They didn’t believe the MRFIT results apparently, so they had a low fat (caloric restricted) arm and a control arm [the SAD diet (Standard American Diet)]. The women on the low fat arm lost a whooping 0.4 kg over the 8 year period (JAMA. 2006 Jan 4;295(1):39-49). 0.4 kg, really!?? That’s almost an entire pound of weight loss over 8 years. Quick, call Barnes & Noble so we can package that diet and sell it on Opra!! (Oh, wait, the news media was a little embarrassed by the findings and never really mentioned them.)
Lastly, if research on 60,000 men and women wasn’t enough to demonstrate what most primary care physicians seen in their offices daily, we had to do the Look AHEAD Study (Action for Health in Diabetes). This study started in 2001 and was supposed to run for 13.5 years. It studied 5,145 Type II diabetic patients with intensive lifestyle intervention. These patients were placed on intensive caloric and fat restriction of 1200-1800 calories per day with exercise and behavioral counseling. It was so unsuccessful, that they stopped the trial at 9.6 years – cause it wasn’t working.
The patients did lose some weight through Look AHEAD . . . an average of 6% of their body fat (That means you would have lost 15.6 lbs over 9 years if you weighed 260 lbs. Successful? . . . NOT). What made this trial worse is that it didn’t improve risk for coronary artery disease and people didn’t live longer (N Engl J Med 2013; 369:145-154). They just got the exciting chance to eat cardboard for 9 years of their lives. Sad. Very sad.
So, what does all this mean? Exercising your brains out at an expensive gym every morning won’t do much more than help you loose 1% of your body fat. It won’t increased your life span and it won’t decrease your risk of heart disease, despite what Dr. Ornish said. If you like spending $40 per month just to stare at sweaty fat bodies jumping up and down in spandex, by all means, please keep going to the gym. But I’d much rather spend that $40 on a nice rib eye steak at a restaurant staring at my wife. But, the benefits of saturated fat . . . that’s for another post.
Don’t get me wrong. I love lifting weights. I love riding my horse. I truly enjoy working in my yard. I even enjoy riding my bicycle. But I do these things now because they bring me peace, decrease my stress, and allow me to connect with nature. Believe me, there’s nothing natural about a 250 pound man in spandex staring at himself in a mirror repetitively lifting 30 pound bars of iron. But, we won’t go there.
My friends, and a few of my patients, get their knickers in a wad trying to decry the fact that I’m giving people a reason not to go running. Maybe I am. To be honest, there’s really only one reason I want to run, . . . and that’s when I’m being chased by a bear. But what good does it do to guilt a person into participation in an activity that isn’t really benefiting their health or help them lose weight, unless they really truly enjoy the activity for the sake of the activity?
Our health is not based upon a caloric scale of inputs and outputs. We are hormonal machines. We gain or lose weight and we gain or lose muscle based on powerful hormone signals, specifically insulin. Simple carbohydrate restriction has profound effects upon our weight, blood pressure, cholesterol and inflammatory states. Until we each come to grips with the fact that the food we eat triggers hormone responses in our bodies, we will continue down the path of diseases of civilization. Hippocrates summed it up when he said, “Let food be thy medicine, and let medicine be thy food.”
Why Your Oatmeal is Killing Your Libido
Have you noticed that there are a large number of advertisements in the media about checking your testosterone or “Low T” Syndrome? It seems like this is the new advertising trend on the radio and late night TV.
Suddenly, everyone’s testosterone is low and men are complaining about their libido, . . . or are they?
If you practice medicine long enough, you’ll see a trend that seems to have arisen as our waistlines have expanded. About half of the men in my office with insulin resistance, pre-diabetes or diabetes have low testosterone levels. But this shouldn’t be a surprise. Type II diabetes, metabolic syndrome and insulin resistance are all driven by an over production in insulin in response to a carbohydrate load in the meal. Patients with these conditions produce between two to ten times the normal insulin in response to a starchy meal. A number of studies both in animal and human models demonstrate that insulin has a direct correlation on testosterone suppression in the blood. This has been demonstrated in both men and women. In fact, glucose intake has been shown to suppress testosterone and LH in healthy men by suppressing the gonadal hormone axis and more predominant testosterone suppression is seen in patient with insulin resistance or metabolic syndrome.
In fact, to put it simply, insulin increases the conversion (aromitization) of testosterone to estrogen in men (it does the opposite in women). Interestingly, Leptin resistance has a similar effect. I tend to see the worst lowering of testosterone in men with both insulin and leptin resistance.
How to you improve your testosterone? Supplemental testosterone has been shown to help, but it comes with some risks, including prostate enlargement and stimulating growth of prostate cancer. The most natural way to improve your testosterone is to change your diet.
A low carbohydrate or ketogenic diet turns down the insulin production and allows the testosterone to be available for use by the body. A ketogenic diet has the effect of reducing leptin resistance as well through weight loss. A simple dietary change of this type is frequently seen in my office to increase testosterone by 100-150 points.
What is a ketogenic diet? It is a diet that restricts carbohydrates to less than 50 grams per day, thereby causing the body to use ketones as the primary fuel source. So, for breakfast tomorrow morning, hold the oatmeal (1/2 cup of Quaker Instant Oatmeal is 31 grams of carbohydrates) and have the bacon and eggs. And, rather than have the cheesecake for desert this evening, have an extra slice of steak butter on your rib-eye and hold the potato.
Math Quiz
Low Carb Chocolate Chip Cookies
Low Carb Chocolate Chip Cookies
I love chocolate chip cookies! However, over the last seven years, as I have followed a low carbohydrate diet I have not been able to indulge my chocolate chip cookie craving — until recently.
Ketogenic Diet Reduces Diabetic Nephropathy
A common problem that arises in patients with diabetes is that of kidney disease or “nephropathy.” Nephropathy is defined as damage to or disease of the filtering system of the kidney. In diabetic patients, they commonly begin to loose the ability to adequately filter and retain microscopic protein needed in the body. As the blood sugar and insulin levels progressively rise over time, damage to the delicate filtering system of the kidneys occur.
Very impressive results revealing improved kidney function were found in both Type I and Type II diabetic mice placed on a low carbohydrate, or ketogenic, diet in just and 8 week period of time. The nephropathy (reduced passage of protein through the kidneys) was completely reversed in all the mice. This is the first in what I suspect will be a series of articles showing that ketogenic diets have significant effect on reversal of age related and diabetic tissue damage. See the article here.