Tag: Inflammation

November 8, 2022

Long COVID, Post Vaccination Syndrome, Clots and the D-Dimer

The COVID-19 spike protein is responsible for serious clotting disorders being seen more and more often. This is happening so much that morticians are now commenting about the record number of “rubber-like” bands being pulled from people’s vascular systems upon starting the embalming process.

Fibrous Clots found in corpses by Richard Hirschman (https://www.theepochtimes.com/health/why-spike-protein-causes-abnormal-blood-clots-200-symptoms_4842684.html)

I’ve personally seen at least 50 cases over the last two years where patients present with profound fatigue, SOB, abdominal pain, diarrhea and extremity pain post vaccination with no really clear explanation in the medical literature until now. Patients exposed or vaccinated are having these symptoms linger for as long as 24 months.

A large scale cohort UK study based on 48 million adults in England and Wales found that in the first week after a COVID-19 diagnosis, the risk of an arterial blood clot was nearly 22 times higher than in someone without COVID-19, and 33 times higher for those with a venous clot condition.

A clot in the artery is the kind that could cause a heart attack or ischemic stroke by blocking blood flow to the heart or brain. That’s different from a clot in the vein leading to a clot in the lung. Though we are seeing both in escalating numbers.

An estimated 10,500 additional cases of clot-related problems, i.e. about 7,200 additional heart attacks or strokes, and 3,500 additional cases of pulmonary embolism, deep vein thrombosis, or other venous problems was identified in this British study alone. Even though that risk drops sharply to less than four times higher than someone without COVID in the second week, it remains high (2x) even up to 49 weeks after the initial diagnosis. This is especially so in regards to the risk of blood clot formation in the legs (deep vein thrombosis or DVTs).

It’s All Due to the Spike Protein

The spike protein that the virus is wrapped in and that the vaccine causes to be replicated in your RNA is the actual trigger for the clotting cascade. It’s the reason I called it the ‘clot shot” last year and now we know it increases clotting in three different mechanisms.

The nasty little virus, SARS-CoV-2, enters our cells via a fancy little protein receptor call the angiotensin-converting enzyme 2 (ACE2). And, not so lucky for them, Endothelial cells (ECs), express an abundance of ACE2. ECs reside on the inner surface of every blood vessel across our entire body, making them a direct target of the virus infection.

Many other cells, including lung epithelial cells, enterocytes lining the small intestines, and cardiac pericytes, all express ACE2.

Spike proteins don’t only activate epithelial cells (EC) and promote localized inflammation. They also promote systemic inflammation as ACE2 is almost everywhere inside our major organs and tissues. And, this coding literally gets written into the DNA.

This leads to more pro-inflammatory genes getting expressed. More and more immune cells are attracted and sent to the injured or infected tissues (vessels in the lung, heart, gut, etc).

A number of downstream events occurs contributing further to the clotting cascade:

Complement-mediated inflammation of epitheliums (endothelialitis): Spike proteins docking on ACE2 ECs activates the complement pathway and coagulation cascade, resulting in a systemic endothelialitis (lung injury) and procoagulant state (tendency to develop blood clots).
As the complement destroys the endothelium, the procoagulant von Willebrand factor (vWF) and FVIII are released. A significant increase of vWF can form multimers that promote thrombus growth. vWF is secreted mainly from endothelial cells and from a-granules of platelets (megakaryocytes derived). This is comparable to the string in the “beads and string” of a necklace where the beads represent platelets.
Platelet storm: Platelets are a small fragment of the megakaryocytes. The complement anaphylatoxins C3a and C5a activate platelets and increase the production of tissue factor further promoting a clotting forming state. ACE2 receptors are present on platelets, and this may contribute to the massive platelet aggregation, which is a characteristic of severe COVID-19 infection.
Activation of neutrophils leads to formation of neutrophil extracellular traps (NETs), a process sometimes referred to as NETosis, which contributes to thrombosis.
EC injury is compounded by toll-like receptor (TLR) activation by viral RNA recognition, with resulting increased reactive oxidative species (ROS) production. The increased ROS further upregulates the expression of vWF. The DNA expression of clotting sensitivity is literally turned up.
Spike proteins can induce expression and secretion of a series of clotting proteins which cascades into the clotting process, including factor (F)-V, thrombin, and fibrinogen to promote clotting process.

Spike Protein Impairs Regulation of RAAS – Leading to More Clots

Now if all of the above wasn’t bad enough, because the spike protein directly interacts with ACE2 expression, COVID-19 patients showed an elevated level of serum angiotensin II indicating a dysregulation of the RAA system (renin angiotensin aldosterone system, or RAAS).

Traditionally, people think angiotensin II is a neurohormone that stimulates the constriction of vascular smooth muscle cells and is responsible for salt and water balance, controlling blood pressure. However, there have been abundant studies supporting the idea that angiotensin II is capable of initiating and upregulating inflammatory responses, worsening the clotting state.

In a normal immune response, these mechanisms help to calm down the local injury, with subsequent healing and returning to a resting EC state.

However, for predisposed COVID-19 patients or vaccinated patient, the factors strengthening clot formation can over power the normal healing mechanisms, all of which lead to an escalating thrombotic cascade.

The Birth of a COVID Clot (it’s like a TV Soap Opera story)

The spike induced endothelial disruption leads to massive amounts of vWF release. Then a subsequent platelet storm happens leading to hypoxia induced upregulation and activation of vWF. What follows is a fibrous network from neutrophil extracellular traps (NETs), as well as increased angiotensin II levels, all adding up to initiate thrombogenesis. In a nutshell, the spike protein drives the formation of the clot through six different dysregulated mechanisms and is the beginning of the long rubbery clots in the arterial system of the body. Furthermore, the upcoming second scene takes another pivotal part in the whole story.

A COVID vaccine instructs the cells to produce large quantities of spike proteins. Normal biochemical and physiological processes are “hijacked” in order to make an abnormal amount of these spike proteins. Again, your DNA is hijacked to make more spike protein. Did you know that?

These abnormal amounts of spike protein have more surprising direct effects on clots.

Spike Proteins Directly Disrupt the Clot Dissolving Mechanism

In a normal healthy person, the body will, in the presence of a blood clot, break the clot down by a process of fibrinolysis. This is a natural healing and balancing mechanism to prevent an abundance of blood clots.

During this process, Tissue Plasminogen activator (TPA, coming from the endothelium) helps plasminogen change into plasmin and then this causes the generation of d-dimer (a small protein fragment left when a blood clot dissolves). This is the flag telling us that the clot dissolving mechanism is broken. This is what I commonly measure every 2-4 weeks in these patients. Interestingly, these patients symptoms resolve once the d-dimer is normal.

Every one of my 50 patients has had D-Dimers elevated for 6-24 months.

It has been discovered that fibrinogen in blood can clot into an abnormal “amyloid” form of fibrin that (like other β-rich amyloids and prions) is relatively resistant to proteolysis (fibrinolysis). This is essential amyloid that is hard to remove.

This has been and is strongly seen in the platelet-poor plasma (PPP) of individuals with long COVID and post vaccination long haul syndrome. What is scary is that the extensive fibrin amyloid microclots can persist.

In a recent study by Grobbelaar published in Bioscience Reports in August 2021, the biomarker S1 (or the intruding part of the spike protein) alone can induce fibrin resistance to fibrinolysis, leading to unopposed microclot formation.

When spike protein S1 was added to healthy PPP, it resulted in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin. These proteins were substantially resistant to trypsinization in the presence of spike protein S1.

Hence, the results suggest that the presence of spike protein in circulation may contribute to the hyper-clotting status, and may cause substantial impairment of the clot dissolving process.

Such lytic impairment may result in the persistent large microclots that people have reported and which have been found in plasma samples of COVID-19 patients.

These microclots block up capillaries, and thus to limit the passage of red blood cells, and hence oxygen exchange, which can actually underpin the majority of these symptoms.

Spike Proteins Form Amyloid-Like Substance

Furthermore, to everyone’s surprise, the spike proteins are identified to present seven amyloidogenic sequences and are able to form amyloid-like substances.

In other words, these spike proteins are similar to those beta-amyloid or tau or alpha-synuclein like substances which may cause neuronal loss in Alzheimer’s or Parkinson’s disease. Their structure makes it easy to form tighter string-like bonded structures with longitudinal twisting as well as cross binding, forming a fibrous-like structure visible under the microscope.

Researchers have found that plasma samples from long COVID patients still contain large anomalous (amyloid) deposits (microclots), which are resistant to fibrinolysis (compared to plasma from controls and diabetes), even after trypsinization (cell dissociation after an enzyme breaks down proteins).

After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. Various inflammatory molecules substantially increased in both the supernatant and trapped in the solubilized pellet deposits of COVID-19, versus that of the control samples.

Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.

Significant abnormal amyloid microclot formation that are resistant to fibrinolysis, increased α2AP, and the surge of acute phase inflammatory molecules may therefore be central contributors in both COVID-19 infection and as well as COVID vaccine-related syndrome.

Spike Protein Inhibits Another Anti-Clot Mechanism

Spike protein just keeps presenting one surprise after another.

It’s been reported that the spike protein can competitively inhibit the bindings of antithrombin and heparin cofactor II to heparin, causing abnormal increase in thrombin (clotting) activity. SARS-CoV-2 spike proteins at a similar concentration (~10 μg/mL) as the viral load in critically ill patients can directly cause blood coagulation and thrombosis in the zebrafish model.

These unexpected negative effects of spike protein on the dissolving process of blood clots, including its amyloid nature, all may be the key contributory factors to the abnormal, lengthy fibrous clots observed in COVID-related conditions.

The Spike Protein Is the Smoking Gun

There is clinical evidence that the SARS-CoV-2 spike protein has been detected in clots retrieved from COVID-19 patients with acute ischemic stroke and myocardial infarction.

Recent research conducted by cardiologists from the University of Colorado sheds light on the crucial role of spike protein in the pathology of COVID and COVID vaccine-related injuries.

They analyzed seven COVID-19 patients and six mRNA vaccinated patients with myocardial injury and found nearly identical alterations in gene profiling patterns that would predispose them to clotting state, inflammation, and myocardial dysfunction.

In other words, regardless of whether the myocarditis was caused by the virus or vaccine, the expression of genes responsible for prothrombotic state was turned on in response to the spike protein, and inflammation and myocardial dysfunction exhibited similar changes.

Based on gene analysis, COVID-19 and post-mRNA vaccine injury have a common molecular mechanism. The altered genes pattern includes down-regulation in ACE2, ACE2/ACE ratio, AGTR1, and ITGA5, and up-regulation in ACE and F3 (tissue factor).

What is more alarming, and not previously reported, is that microvascular thrombosis has been found in post-vaccinated patients, indicating that spike protein itself is able to trigger blood clots in susceptible patients.

The Tip of the Iceberg?

Unfortunately, this may only be the beginning. The AstraZenica COVID adenovirus (ChAdOx1-S) vaccine pulled from the marked caused antibody (auto-immune) formation to platelet factor 4 (PF4). Auto-immunity can take years to form before it is recognized.

These unusual blood clots in combination with thrombocytopenia were reported predominantly in women aged under 60 years. Accordingly, several European countries restricted the use of adenovirus vaccines in younger age groups.

This risk has been recently systematically analyzed in an international network cohort study from five European countries and the United States, confirming pooled 30 percent increased risk of thrombocytopenia after a first dose of the ChAdOx1-S vaccine, as well as a trend towards an increased risk of venous thrombosis with thrombocytopenia syndrome after Ad26.COV2.S (the Janssen COVID vaccine) compared with BNT162b2 (the Pfizer-BioNTech COVID vaccine).

What Works to Detoxify the Spike Protein?

I’ve listed my go-to medications below in the order of effectiveness in my clinical experience.

Ivermectin – Ivermectin is a compound that originated from nature. Satoshi Omura, a Japanese microbiologist and organic chemist, who grew up in a farmer’s family, discovered from soil samples the predecessor compound of ivermectin, Streptomyces Avermectinius, and modified it into ivermectin.

Ivermectin has been in use for more than 50 years. Ivermectin was first used in the treatment of parasitic diseases, such as onchocerciasis, river blindness, and elephantiasis.

In addition to treating parasites, in vitro cellular experiments have revealed that ivermectin has broad-spectrum antiviral effects. It can be used to fight against RNA viruses (including HIV, the dengue fever virus, influenza viruses) and DNA viruses.

In addition, ivermectin has a variety of antiviral mechanisms. It can also inhibit viral entry into cells and viral protease function, thus blocking viral replication.

A study published in the journal In Vivo found that ivermectin might interfere with the attachment of spike protein to the human cell membrane.

In an in vitro study on ivermectin published in Antiviral Research, the researchers added ivermectin to cells infected with the SARS-CoV-2 virus and then harvested the supernatant and cell pellets for further analysis. It was revealed that within 48 hours of adding 5 μM ivermectin, the viral SARS-CoV-2 RNA was reduced by 99.999 percent, leaving only 0.001 percent.

A prospective, observational study of the citywide COVID-19 prevention with ivermectin program was conducted between July 2020 and December 2020 in Itajaí, Brazil.

In the absence of contraindications, ivermectin was offered as an optional treatment to be taken for two consecutive days every 15 days at a dose of 0.2 mg/kg/day.

Of the 223,128 citizens of Itajaí considered for the study, a total of 159,561 subjects were included in the analysis: 113,845 (71.3 percent) regular ivermectin users and 45,716 (23.3 percent) non-users. The main findings are: The regular use of ivermectin at 0.2 mg/kg/day for 2 days every 15 days led to a 68 percent reduction in COVID-19 mortality (0.8 percent versus 2.6 percent among ivermectin non-users; p < 0.0001). There was a 56 percent reduction in hospitalization rate (p < 0.0001).

Minocycline – Doxycycline or Minocycline may stop the cytokine storm produced by this segment of spike protein superantigen activity ( Francini E, Miano ST, Fiaschi AI, Francini G. Doxycycline or minocycline may be a viable treatment option against SARS-CoV-2. Med Hypotheses 2020;144:110054. doi: 10.1016/j.mehy.2020.110054. Available at: https://tinyurl.com/bddyrfx2. Accessed May 19, 2022.)

Colchicine – (Colcrys) for pericarditis: colchicine is indicated for the treatment and prevention of gout, though it is also generally considered first-line treatment for acute pericarditis, as well as preventing recurrent episodes. Colchicine has been effective in lowering the d-dimer through it’s effect on improving inflammatory cascades. Although the exact mechanism of colchicine is not fully understood, its anti-inflammatory effect for pericarditis appears to be related to its ability to inhibit microtubule self-assembly, resulting in decreased leucocyte motility and phagocytosis Colchicine is a nonsteroidal antimitotic drug that blocks metaphase by binding to the ends of microtubules to prevent the elongation of the microtubule polymer. This agent has proven useful in gout and idiopathic recurrent pericarditis. The GRECCO-19 randomized open-label trial in 105 hospitalized patients with COVID-19 found that colchicine was associated with a reduction in D-dimer levels and improved clinical outcome.

NAC (N-acetyl-L-cysteine) – This drug is a well-established expectorant, which is able to reduce the stickiness of sputum, as well as an antioxidant.

Although it’s unable to interfere with the binding of spike proteins to ACE2 receptors, it reduces the oxidation of spike proteins after they enter the cells. As a neutralizing agent, it can reduce the consequences of toxicity after poisoning.

A cell model study published in the journal Circulation Research found that the expression of some normal proteins, such as phospho angiotensin-converting enzyme (pACE2), ACE2 and AMP-activated protein kinase (AMPK), decreased in pulmonary artery endothelial cells infected with pseudo-spike proteins, while the expression of the bad protein MDM2 (which promotes tumor formation) increased.

NAC, on the other hand, has a restorative effect on cells. It’s able to restore cells damaged by spike proteins to almost the same state as normal cells.

As there is no direct clinical trial data to confirm the effects on reducing the spike protein toxicity, an instruction under a doctor’s advice must be followed.

Catechin and Curcumin- Catechin, a tea extract, is a natural antioxidant that accounts for about 75-80 percent of the polyphenol content of tea and is one of the sources of the bitterness of tea.

Curcumin, derived from turmeric, is an important component of curry. Curcumin has powerful antioxidant and anti-inflammatory properties.

An article published in Scientific Reports – Nature studied these two components and found that curcumin binds to the receptor-binding domain of spike proteins; and catechin binds to amino acids near the receptor-binding domain, thus blocking spike proteins from binding to the ACE2 receptors and blocking spike proteins from entering cells.

These two ingredients can inhibit viral invasion of cells at the body’s first natural immune barrier, guard the cell’s gateways and offset the strength of the virus.

Carpenter’s Herb – Carpenter’s herb (Prunella vulgaris) has long been considered an effective medicine for liver health.

In 2021, a study by Canadian infectious disease researchers was published in the Public Library of Science: General (PLOS ONE). It proved that the water-soluble extract NhPV of the natural plant carpenter’s herb can inhibit the SARS-CoV-2 and block it from infecting cells. Some other herbs, such as pine needles, emodin, neem, and dandelion leaf extract, are also mentioned in the WCH guidelines as having similar effects in relieving the toxicity of spike proteins. Increasingly, scientific studies are finding that there are more herbal ingredients that have inhibitory effects on the SARS-CoV-2 and can repair the damage caused by vaccination. For instance, scientists have selected 25 candidate compounds from the giant knotweed (Reynoutria sachalinensis) and docked them into the binding site of Mpro, the main protease of SARS-CoV-2. They discovered that 11 of these compounds were effective in inhibiting the replication and transcription of the SARS-CoV-2 virus.

Suramin – Suramin is a century-old medicine that was also first used to treat the parasitic worm disease called onchocerciasis. In addition to treating parasitic diseases, it has been proven effective in inhibiting the replication of many viruses, including enterovirus, Zika virus, and Ebola virus.

Most of the data on Suramin are derived from the in vitro studies. In theory, it should work for reducing the spike in protein toxicity. As there is no clinical trial data to confirm the effects on reducing the spike protein toxicity, an instruction under a doctor’s advice must be followed.

Both ivermectin and suramin can interfere with the binding of spike proteins to ACE receptors and relieve the cellular damage caused by spike proteins.

My hopes in publishing this is that someone, somewhere will benefit and reduce their risk for clot, heart attack, stroke and/or death.

September 28, 2022

Autoimmunity Resulting from Molecular Mimicry between COVID Vaccine and Human Proteins

I’ve been seeing this for two years, elevated d-dimers, blood clots, myocarditis, spontaneous colitis non-responsive to anti-biotics, sudden spontaneous bruising and bleeding after vaccination. Now, it all makes more sense.

In a recent study, researchers discovered molecular mimicry hotspots in the Spike protein and highlight two examples with very high autoimmune potential. This helps us understand the prolonged COVID-19 complications we’ve been seeing for the last two years. The spike protein shares similarities with 34 different human proteins in amino acid sequences in sets of sixes. These similarities stimulate high potential for autoimmune attack – causing the body’s immune system to attack its own organs with similar protein sequences.

These protein sequences are found in the thyroid, brain, nose, ear, skin, muscles, heart, blood, nerves, joints, intestines, and many more. In my office, I’ve seen over 50 patients with bleeding, bruising, rash, heart inflammation, intestinal inflammation, uterine and ovarian inflammation and abnormal menstrual changes spontaneously that I have never seen in 22 years of medical practice. All of these patients have had prolonged d-dimer levels elevated for 12-18 months post vaccination. These symptoms all started with in 4-8 weeks of vaccination as well.

The spike protein may also trigger Guillain-Barre syndrome, viral arthritis, immune thrombocytopenic purpura (bleeding), antiphospholipid syndrome, Kawasaki disease, systemic lupus erythematosus, and many others.

Two other recent studies here and here confirm that autoimmunity is the driver behind these post COVID vaccination symptoms. These two studies demonstrated that people who were vaccinated for COVID-19 had more antibodies against human tissues than people who were not infected and/or had natural infection.

August 12, 2018

Is Keto For Everyone? Dr. Nally’s Three Principles of Health

Is a Ketogenic Lifestyle What Everyone Needs?

“Do I really need to be doing that ‘Keto Thing’?”

I get asked this question all the time. And, my answer is that 85% of the people that walk through the doors of my clinic will not be fully successful in weight loss, reversal of diabetes, normalization of blood pressure and reversal of heart disease and/or vascular disease without it.

I am frequently asked, “Is Keto for everyone?” Does everyone need to follow a ketogenic lifestyle? The answer is “No.” 15% of the population will be able to maintain great health with calorie restriction and exercise. However, the principles that provide a successful ketogenic lifestyle are easily understood and incorporated by anyone looking for improved health, energy and weight control.

Principle #1 – Insulin is the Master Hormone

Insulin is the master hormone when it comes to weight loss and the diseases of civilization. Whether you are insulin resistant or not, insulin is essential for life and proper function of the cells of the body, but too much insulin production in response to sugars, starches or complex carbohydrates causes disease.

How do you know if you are insulin resistant (producing too much insulin)?

Skin tags are pathognomonic (a characteristic indicative of the presence of disease) for insulin resistance. If you have skin tags, you may want to focus your diet on increased carbohydrate restriction.

You may not need to completely remove carbohydrate from your diet, however, recognizing that not all carbohydrates are created equal and avoiding those with higher carbohydrate content will help many improve weight and halt the progression of disease. I have many patients that with just partial carbohydrate restriction they are able to lose 20-30 lbs, improve their cholesterol profiles and improve their blood pressure.

There are sixteen different diseases that respond very effectively to carbohydrate restriction. You can read about them and how the ketogenic lifestyle effectively reverses them in The Keto Cure.

Principle #2 – Saturated Fat & Cholesterol Aren’t the Demons We’ve Made Them Out to Be

Saturated Fat and cholesterol aren’t the demons we’ve made them out to be. Another way to put it is: “Don’t blame the butter for what the bread did.”

Since 1984, nutrition experts treat fat and cholesterol containing foods like the witches of Salem. Experts castigate their use as if they were the “Avada Kedavra“ curse of the fantasy world.

As an example, eggs, specifically the egg yolk (the part of the egg containing all the cholesterol and saturated fat), have been demonized by just about every health magazine I’ve ever read. (To this day, the chef at every breakfast bar I’ve ever visited asks if I want an ‘egg white only’ omelet.) Interestingly, there is actually no scientific data association between whole egg consumption and heart disease. The science simply does not exist. Seriously, check for yourself.

I personally eat 6-8 eggs a day and my cholesterol is perfect. Back 1000 years ago, only the aristocrats at the chickens. All laborers and serfs ate the eggs . . . who would be dumb enough to eat your food source? (Don’t answer that.)

For example, the MR-FIT study, the largest cholesterol 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 stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”

Researchers found that people who ate the most cholesterol, including the most saturated fat, weighed the least. They were also the most physically active. In fact, the British Medical Journal published a 2015 study demonstrating that saturated fat is NOT linked to vascular disease, diabetes or increased mortality (de Souza RJ et al., BMJ 2015,351:h3978).

In my clinic, the basis of appetite suppression is eating adequate protein that includes saturated fat and cholesterol. This is the most powerful tool in my clinical approach to the treatment of weight loss. I can use foods like red meat, bacon, butter and coconut oil without concern or worry of heart disease as long as you are keeping your carbohydrate intake less than 20 grams per day.

Baseline insulin levels allow for peace of mind about heart disease risk. Heart disease risk goes down when insulin levels are maintained at normal baseline levels. Increasing saturated fat, while at the same time lowering carbohydrate intake has been demonstrated to shift the cholesterol to a more heart protective form (Griffin BA et al., Clin Sci [Lond], 1999 Sep).

Principle #3 – Nutritional Ketosis Has Anti-Inflammatory & Age Slowing Effects On the Body

Ketones in the blood at a nutritional level (0.5-4 mmol/L) have tremendous anti-inflammatory and age slowing effects on the body. Even having them present intermittently has dramatic improvement on overall inflammatory changes and disease in the body.

Ketones are the usable fuel of the body when the liver breaks down fat for energy. They suppress the NLRP3 inflammasome in every cell in the body. This is important because it allows for more rapid recovery from exercise. It also dramatically decreases pain and fatigue that comes from diseases like arthritis, rheumatoid arthritis, multiple sclerosis and auto-immune disease (Y.H. Youm, et al., Nature Medicine, vol. 21, no. 3, pp. 263–269, 2015.)

If full blown ketosis isn’t for you, partially restrict starch and carbohydrates for a mild to moderate benefit. Even small amounts of ketones in the blood are helpful. This provides increased recovery time, and improved inflammation control.

So, even if you don’t follow a strict ketogenic lifestyle, the principles above are powerful. These three principles make this dietary approach universally effective for weight loss. They are also very powerful for disease management. Even partial application of carbohydrate restriction can benefit just about everyone.

You can learn much much more about the Ketogenic Lifestyle as a member of DocMuscles.com. Click the link and sign up now.

And, don’t forget to get your signed copy of my book, The Keto Cure.

September 27, 2016

The 25 Benefits of Ketosis . . . Other than Fat Loss: Part I – Inflammation

Stay tuned for Part II – Gut hormones & GLP-1.

April 21, 2016

Can You Gain Muscle On A Ketogenic Diet?

Listen in to Ketotalk Podcast #19 where we talk about inflammatory foods, building muscle with a ketogenic diet & how ketosis affects the Baby Boomer Generation.

Keto Talk is cohosted by 10-year veteran health podcaster and international bestselling author Jimmy Moore from “Livin’ La Vida Low-Carb” and Arizona Osteopath and Board Certified Obesity Medicine physician Dr. Adam Nally from “Doc Muscles” who thoroughly share from their wealth of experience on the ketogenic lifestyle each and every Thursday.

We love hearing from our fabulous Ketonian listeners with new questions–send an email to Jimmy at livinlowcarbman@charter.net. And if you’re not already subscribed to the podcast on iTunes and listened to the past episodes, then you can do that and leave a review HERE. Listen in today as Jimmy and Adam answer more engaging questions about nutritional ketosis from you the listeners.

April 9, 2016

Is Ketosis Really Bad For You?

A patient recently asked me how bad being in nutritional ketosis was for her. I responded that the worse problem I’ve seen recently is the patient that broke his toe when he slipped on bacon grease. Are there risks with a ketogenic diet? Yes, but these usually only occur when you cheat or fall off the wagon. What problems can arise? Lets talk about them individually.

First, as I stated above, make sure you don’t slip on bacon the grease. It really can be an issue if you’re not used to using increased amounts of fat in your kitchen. So, be prepared for how to cook and use fat. Grandma understood this well, we could learn a great deal from her if you ask her about using bacon grease.

Second, let’s define the difference between ketosis and keto-acidosis and try to clarify the misinformation that is being spread around the blogosphere.

A ketone is a molecule the body produces from the breakdown of fat (specifically triglycerides) and some proteins (amino acids). There are specifically three types of ketones: beta-hydroxybutyric acid, acetoacetic acid and acetone. If ketosis was “bad,” then why would our bodies produce these molecules? They are not bad, and in fact, multiple studies show that the body is often more efficient in weight loss, inflammatory reduction, bowel function, epigenetic influence and maintenance of lean body mass more effectivly when it functions on ketones rather than glucose as its primary fuel source. You can see these studies here, here, here and here.

The body can only supply a limited amount of sugar or glucose for fuel. If you talk to runners, marathoners or triathletes, they will tell you that after about 45-90 minutes of continuous endurance exercise the glucose supply runs out and they will experience what is termed a “bonk” (have a low-blood sugar or hypoglycemic episode). Unfortunately, our bodies can only store about 18-24 hours of glucose.

However, the body can store days upon days of fat in the form of triglyceride in the fat cells. Triglyceride is broken down into ketones. If glucose is the “unleaded” fuel, you can think of ketones as the “diesel fuel” that is easier to store and runs longer.

The average body functioning on ketones as the primary fuel will have a ketone level measured in the blood somewhere between 0.4 and 4 mmol/L. Because of a balance that is created by the use of ketones and a feedback mechanism that kicks in when the ketone level rises, the body will maintain a pH of around 7.4.

Ketoacidosis is dramatically different. If you are a type I diabetic, you don’t produce any insulin. The feedback mechanism regulating ketone use is broken and the ketone levels and triglyceride breakdown speeds up because the body can’t access glucose and can’t produce insulin. The ketone levels spike and the level can rise to > 25 mmol/L. In the presence of a high blood sugar and high ketone level, the acid level in the blood shifts to a pH of less than 7.3. This is referred to as metabolic acidosis and can be life threatening as the low pH shuts down the bodies’ enzymatic processes and a person becomes critically ill and without treatment, can die. Further information on ketoacidosis can be found here.

If you’re not a type I diabetic, you have nothing to worry about. Regardless of what the “ketogenic nay-sayers” blog about, your liver makes approximately 240g of glucose per day, 24 hours a day, 7 days per week, this stimulates a basal release of insulin which keeps the pH in check. It’s also what keeps weight loss at a consistent pace of around 2-10 lbs per month.

If you are a type I diabetic, don’t fret. Carbohydrate restriction can still be used very effectively. It just takes some balancing and understanding of your individual metabolism. It does require close blood sugar and insulin monitoring. If you are a Type I diabetic, please talk to your physician, obesity specialist and/or bariatrician about how to follow a carbohydrate restricted diet while using insulin. It can be done and it can be done very effectively, but monitoring is essential.

What are the other potential problems that can arise when you follow a ketogenic diet?

Gastrointestinal (GI) Disturbances – Yes. Any time you change your diet you may experience diarrhea, constipation or gassiness. Most of the time, this is because you are either 1) not eating enough leafy greens (fiber) or 2) you’re using a supplement that contains an artificial sweetener. Most of the studies on ketogenic diets did not incorporate fiber and the studies used to make this point were on children who used a ketogenic fat supplement shake or liquid preparations containing these artificial sweeteners to make them palatable. If you have spoken to any obesity specialist, they will tell you, the best way to follow a ketogenic diet is to eat real food. If you want to read about the anecdotal GI effects of sweeteners, read the comment section in Amazon about the Haribo Sugar Free Gummy Bears.

Oh, by the way, 65% of patients in my practice following ketogenic diet see improvement in gastroesophageal reflux (GERD) symptoms. This was seen in a 2006 study looking at ketogenic diets and reflux.

Hair Loss/Thinning – Yes. This does happen initially and if you are not eating enough fat. It is important to note that hair loss/thinning can occur with any form of weight loss. You can see data on this here. Hair loss is very common if you are restricting calories, which was occurring in a number of the ketogenic dietary studies previously published. You do not, and should not, need to “restrict calories” if you are following a ketogenic diet correctly, and in fact, most people take in more than 1800 calories on a ketogenic diet.

Inflammation Risk – In every patient that I have placed on a ketogenic diet in the last 10 years, all inflammatory markers including CRP, Sedimentation Rate, Apo B, HOMA-IR and Uric Acid have all decreased. Inflammation gets better on an appropriately formulated ketogenic diet. The older studies of ketogenic diets in children contain most of their fat from Omega-6 fatty acids from vegetable oil which will increase inflammation and oxidative stress, spike the cortisol levels and have the secondary effect of actually raising the triglycerides. You can find more information on this here & here.

Kidney Stones/Gout – These (kidney stones & gout) are both commonly caused by spikes in uric acid. As noted above, I’ve seen multiple cases in my practice where a ketogenic diet lowers uric acid. Only a small clinical trial has been published in the literature (and it wasn’t truely ketogenic), but the results point to the potential for ketogenic diets to lower uric acid. Ketogenic diets also have the capacity to lower the formation of calcium oxalate stones through a secondary mechanism where calcium oxalate formation is driven by uric acid formation. Older small case reports in the pediatric seizure literature identify calcium oxalate stones, however, dehydration (too little fluid/water intake) is the primary cause of kidney stones.

So, are ketogenic dietary patients at risk? Only if you cheat on your carbohydrate restriction and you let yourself get dehydrated. So, I warn patients. Don’t cheat and make sure your drinking adequate amounts of water.

Muscle Cramps/Weakness – The process of weight loss occurs by burning fat into CO₂ and water. We breathe the CO₂out, but the water produced has to follow salts out through the kidneys. Hence, we lose water and salts. This can cause weakness and muscle cramps. The solution? Stop restricting salt on a low carbohydrate diet. We are the only mammal that restricts salt and we do it because low-fat diets cause us to retain water. Low carbohydrate diets do the opposite. Use sea salt or sip beef or chicken bouillon broth with your dinner. You may consider adding magnesium to your diet. The use of yellow mustard also helps (the small amount of quinine in yellow mustard stops the cramping). If you have congestive heart failure, talk to your doctor about monitoring your salt intake in balance with your diuretic or water pill.

Hypoglycemia – If you read the ketogenic diet research, most of it was done on epileptic children. The diets called for a period of starvation, and then the introduction of a ketogenic liquid based shake following the John’s Hopkin’s protocol. It is a well-known fact in medicine that starvation in children can frequently cause hypoglycemia, especially in children with other genetic or congenital defects leading to forms of epilepsy. In clinical practice, with ketogenic diet use in adults, hypoglycemia is rare. The only time I see hypoglycemia is when patient’s with significant insulin resistance or diabetes cheat on a large amount of carbohydrate and get a secondary insulin surge leading to hypoglycemia 3-5 hours after cheating.

Low Platelet Count (Thrombocytopenia) – Again, this was seen in epileptic children who were placed into starvation first, then introduced a liquid fat replacement shake to stop intractable seizures. These liquids or shakes were often nutrient deficient in other essentials. Folic acid, B12 and copper deficiency can occur when not eating “real food.” Low platelet counts are rarely seen on ketogenic diets based around “real food.” Many children in the ketogenic studies had been on or were concomitantly on valproic acid for their seizures. Valproic acid is commonly known to cause thrombocytopenia and this is another reason that thrombocytopenia was seen in this population. (Barry-Kravis E et al, Bruising and the ketogenic diet: evidence for diet-induced changes in platelet function. Ann Neurol. 2001 Jan;49(1):98-103.; Kraut E, Easy Bruising, http://www.uptodate.com, May 2015.)

Impaired Concentration/Mood – A number of patients starting carbohydrate restriction will go through 2-4 weeks of carbohydrate withdrawal. This carbohydrate withdrawl can be experienced just as powerfully as morphine withdrawal in some patients. Sugar is a drug and has a powerful effect on the same hedonic receptors that morphine does in the brain. Some patients will experience headache, tremor and decreased concentration while “withdrawing” off of starches and carbohydrates. Studies show that after the 4-8 week period of keto-adaptation, cognitive function dramatically improves.

Metabolic Acidosis – As described above, metabolic acidosis can occur in a type I diabetic who is not getting adequate insulin, and metabolic acidosis has also been shown to occur in young children placed on severe carbohydrate AND protein restriction, as was the case in some of the ketogenic dietary trials with epileptic patients. (Saxena VS, Nadkarni VV. Nonpharmacological treatment of epilepsy. Annals of Indian Academy of Neurology. 2011;14(3):148-152. doi:10.4103/0972-2327.85870.; Freeman, et al., The Ketogenic Diet: One Decade Later, Pediatrics March 2007; 119:3 535–543).

Osteoporosis/Osteopenia – If your ketogenic diet is “shake” or “meal replacement” based, you run the risk of mineral deficiency that could lead to Osteoporosis, however, if you are using real food, the opposite is true and most patients have improvement in their Vitamin D levels and bone density. (AG Christina Bergqvist, Joan I Schall, Virginia A Stallings, Babette S Zemel, Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic dietAm J Clin NutrDecember 2008 88: 1678–1684; doi:10.3945/ajcn.2008.26099)

Easy Bruising – This is usually due to inadequate protein supplementation as was the case in much of the ketogenic literature where protein levels were also restricted. (Kraut E, Easy Bruising, http://www.uptodate.com, May 2015.)

Infections/Sepsis/Pneumonia – Increased susceptibility to illness has never been an issue in the 10 years I have been using ketogenic diets with my patients. These issues were seen in the John’s Hopkins protocol with children who had not only epilepsy, but other congenital disorders predisposing them to infection, who were placed on a diet low in protein and carbohydrate. (Saxena VS, Nadkarni VV. Nonpharmacological treatment of epilepsy. Annals of Indian Academy of Neurology. 2011;14(3):148-152. doi:10.4103/0972-2327.85870.)

Pancreatitis – Patients who are insulin resistant or have impaired fasting glucose commonly have high triglycerides. Elevation in triglycerides itself is a cause of pancreatitis. Ketogenic diets lower the triglycerides. However, if a patient has not been following their diet as directed, spikes in the triglycerides can occur placing the person at risk for pancreatitis.

Long QT Intervals/Heart Arrhythmias – The list of things causing Long QT intervals and abnormal heart rhythms is long and variable (Acquired Long QT Syndrome. Berul C et al. www.uptodate.com, May 2015). It is well know that starvation, rapid weight loss and liquid protein diets can cause a delay in the conduction signal in the heart. Anyone wishing to start any diet should have an electrocardiogram (EKG) through their doctor to ensure that the diet (of any type) doesn’t exacerbate a prolonged QT interval.

Cardiomyopathy – Prolonged QT intervals have been associated with cardiomyopathy and the former can stimulate the later. Any diet that has the potential to prolong a QT interval has the potential to cause cardiomyopathy. Hence the need for regular EKG monitoring on any diet (Acquired Long QT Syndrome. Berul C et al. www.uptodate.com, May 2015).

Lipid/Cholesterol Changes – In the 10 years I have been prescribing ketogenic diets to patients, I have seen dramatic improvement in the triglycerides, small dense LDL particle and HDL levels. The only time triglycerides rise over 100 is if the patient is using artificial sweeteners, is cheating on the carbohydrate restriction, or is taking in too much protein. Total cholesterol commonly rises, however, this is indicative of the fact that there is a shift in the LDL particle size and this affects the calculation of both total cholesterol and LDL-C. In light of this, most of my patients have dramatic improvement in triglycerides and small dense LDL particle number.

Myocardial Infarction – In older papers, elevated total cholesterol was noted and the authors made the “assumption” that myocardial infarction “could” be a risk. We now recognize that elevated Total Cholesterol is NOT a causitive risk for heart disease.

These previous assumptions have been interpreted by the blogosphere ketogenic “nay-sayers” as actual risk. However, a correlation and causation was never made. Again, in the 10 years I have been using and prescribing ketogenic diets, I have seen dramatic improvement in cholesterol profiles, inflammatory markers, atherosclerosis and carotid intimal studies (Shai I et al, Circulation 2010; 121:1200-1208).

Menstrual Irregularities / Amenorrhea – It is well known that any diet causing protein or other nutritional deficiency will affect the menstrual cycle first and growth in stature second. The only time menstrual irregularities occur with a ketogenic or Low-Carb diet is when a patient is not taking in enough protein and/or fat, and is not eating real food. What amazes me is that a properly applied ketogenic diet actually causes normalization of the menstrual cycle, and in my practice, I’ve had a number of women successfully be able to conceive after making a ketogenic dietary change.

Death – All cases of death related to ketogenic diets have been documented in children while using liquid based carbohydrate and protein restricted formulas for ketosis to treat epilepsy. These cases revealed the formation of a prolonged QT interval leading to cardiomyopathy due to deficiency in selenium. This was later solved by the addition of selenium to the ketogenic supplement. (Stewart WA et al., Acute pancreatitis causing death in a child on the ketogenic diet, J Child Neurol. 2001 Sep;16(9):682.; Bergqvist AG et al, Selenium deficiency associated with cardiomyopathy: A complication of the ketogenic diet. Epilepsia. 2003 Apr;44(4):618-20.; Kang HC et al., Early and lat onset complications of the ketogenic diet for intractable epilepsy, Epilepsia. 2004 Sep;45(9):1116-23.; Kang HC et al, Efficacy and Safety of the Ketogenic diet for intractable childhood epilepsy: Korean Multicentric Experience, Epilepsia. 2005 Feb;46(2):272-9.) Selenium deficiency does not happen when the diet is based on the use of real food instead of supplementation, and has never been seen in adults.

Is a ketogenic diet bad for you? You be the judge.

If you are following a ketogenic diet correctly and with real food, the only thing you really need to worry about is slipping on bacon grease.

In an era where over 70% of us (35.7% obesity & 34% overweight in 2015 according to the CDC) have started to resemble the food pyramid, seeing the effect of a carbohydrate heavy diet should give a clue.

Our bodies were meant to burn ketones. We have a parallel system within us designed to use ketones as an energy source. Ketones are faster and more efficient than the way our bodies use glucose. Ketones give you 38% more energy than you can get from glucose. We as a society are following a deceptive food pyramid.

When we limit or remove carbohydrate from our diet, we are left with ketones as a primary fuel. It is time that we recognize what Dr. Yudkin was trying to tell us in 1970’s, that our carbohydrate and sugar intake is the driver for heart disease, diabetes and the diseases of civilization. (Yudkin, John. Sweet and dangerous: the new facts about the sugar you eat as a cause of heart disease, diabetes, and other killers. PH Wyden, 1972.)

KetoOS – Drinkable Exogenous Ketones

September 10, 2015

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

May 10, 2015

Much Ado About Ketosis: Are The Adverse Effects Really That Adverse?

I recently read a blog post decrying anyone that would recommend a low carbohydrate / ketogenic diet to their patients.

What?!

In fact, this particular blog outlined a number of “adverse reactions” to a ketogenic diet, and based upon these perceived reactions, the writer advised severe caution with its use in just about anyone. It is important to note at the outset that most of the data this blogger quotes are from older studies completed in children for the treatment of epilepsy with specific liquid ketogenic dietary meal replacements. (Not what you’d expect in a low-carb / ketogenic diet for the average obese adult today.)

Diet Confusion

Thanks to recent misinformation by a number of medical professionals, including the person writing the blog referenced above, a poor understanding of fatty acid metabolism by the general community, and a distinct lack of understanding of human adaptability recorded over the last 5,000-6,000 years, there is still significant confusion about ketogenic diets.

It is important to recognize the crucial fact that the human body is designed to function quite well when supplied any of three macronutrients: carbohydrates, proteins or fats. It does so through an amazing series of enzymatic reactions referred to as the Krebs (tricarboxylic acid) cycle, producing needed ATP (adenosine triphosphate) required for our muscles to contract, our heart to beat and our diaphragm to expand our lungs. What’s even more amazing that that the body was designed to recognize the season we are in based up on the food we eat. That is, until we invented refrigerators in 1913. (Now our bodies think it’s year round summer time . . . wait . . . I live in Arizona where it is year round summer time.)

No, this is not a post about unplugging your refrigerator, living on solar, getting off the grid and saving energy.

Our bodies recognize the seasons we are in based upon inherent hormone release. The key hormone is insulin. Insulin can be looked at as the seasonal indicator to our bodies. Insulin production rises and falls based on our intake of carbohydrates (sugar, starches, some fibers). Insulin, essentially, tells our bodies when it is a “time of plenty” and when it was a “time of famine.” Why? You ask. We didn’t have refrigerators 100 years ago and you were lucky if you had a root cellar. The body needs to know when to store for the famine (the winter) that was around the corner. Insulin is that signal.

During the summer, potatoes, carrots, corn and other fruits are readily available. These are all starchy carbohydrates and they all require the body to stimulate an insulin response so that they can be absorbed. Insulin stimulates fat storage (J Clin Invest. 2000;106(4):473-481. doi:10.1172/JCI10842). Just like bears, our bodies were designed to store for the winter.

During the winter, when carbohydrates were less prevalent, insulin production could and would decrease to baseline levels. This also is a natural phenomenon that occurs with fasting and even during lactation. (Kreitzman SN. Factors influencing body composition during very-low-caloric diets. Am J Clin Nutr. 1992;56(l Suppl):217S–23S.; Medical aspects of ketone body metabolism. Mitchell GA, Kassovska-Bratinova S, Boukaftane Y, Robert MF, Wang SP, Ashmarina L, Lambert M, Lapierre P, Potier E, Clin Invest Med. 1995 Jun; 18(3):193-216.)

If you think back in history, your grandparents probably used stored meats & cheeses that could be salted or smoked for preserving during this time of year. Those crossing the plains were commonly found with pemmican, a concentration of fat and protein used as a portable nutrition source in the absence of other food. (Chapter VIII. Narrative of the Life of David Crockett, of The State of Tennessee, Written by Himself, Sixth Edition [E.L. Carey and A. Hart:Philadelphia] 1834, 1837; Marcy, The Prairie Traveler, p. 31.) Think about conversations you may have had with your grandmother when she told you that for Christmas, she received an orange. A single orange for a gift?! Many of my patients drink 12-15 of them in a glass every morning. The winter diets of our grandparents were very low in starches and carbohydrates. When carbohydrate intake is low, little insulin is produced.

Again, insulin is the hormone that tells you that you’re in “a time of plenty” and stimulates weight gain and cholesterol production to prepare for winter. Those prescribing the use of ketogenic diets understand this innate human adaptive trait, and use it to effect changes in weight, cholesterol and other desired metabolic changes.

Three types of ketones. Uptodate.com, May 2015

Now, let’s define the difference between ketosis and keto-acidosis and try to clarify the misinformation that is being spread around the blogosphere.

A ketone is a molecule the body produces from the breakdown of fat and some proteins (amino acids). There are specifically three types of ketones: beta-hydroxybutyric acid, acetoacetic acid and acetone. If ketosis was “bad,” then why would our bodies produce these molecules? They are not bad, and in fact, multiple studies show that the body is often more efficient and effective when it functions on ketones rather than glucose as its primary fuel source. The body can only supply a limited amount of sugar or glucose for fuel. If you talk to runners, marathoners or triathletes, they will tell you that after about 45-90 minutes of continuous endurance exercise the glucose supply runs out and they will experience what is termed a “bonk” (have a low-blood sugar or hypoglycemic episode). Unfortunately, our bodies can only store about 18-24 hours of glucose.

Metobolic Changes of Ketogenic Diet (American Journal of Physiology – Endocrinology and Metabolism Published 1 June 2007 Vol. 292 no. 6, E1724-E1739 DOI: 10.1152/ajpendo.00717.2006)

Ketoacidosis is dramatically different. If you are a type I diabetic, you don’t produce any insulin. The feedback mechanism regulating ketone use is broken and the ketone levels and triglyceride breakdown speeds up because the body can’t access glucose and can’t produce insulin. The ketone levels spike and the level can rise to > 25 mmol/L. In the presence of a high blood sugar and high ketone level, the acid level in the blood shifts to a pH of less than 7.3. This is referred to as metabolic acidosis and can be life threatening as the low pH shuts down the bodies’ enzymatic processes and a person becomes critically ill and without treatment, can die. (Kitabchi AE et al., Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. www.uptodate.com, May 2015.)

If you’re not a type I diabetic, you have nothing to worry about. Regardless of what the “ketogenic nay-sayers” blog about, your liver makes approximately 240g of glucose per day, this stimulates a basal release of insulin which keeps the pH in check. It’s also what keeps weight loss at a consistent pace of around 2-10 lbs per month.

What about all the other “adverse effects” the blogosphere and other so-called experts claim about ketogenic diets?

Let’s take them on one by one. Are you ready?

Gastrointestinal (GI) disturbances – Yes. Any time you change your diet you may experience diarrhea, constipation or gassiness. Most of the time, this is because you are either 1) not eating enough leafy greens (fiber) or 2) you’re using a supplement that contains an artificial sweetener. Most of the studies on ketogenic diets did not incorporate fiber and the studies used to make this point were on children who used a ketogenic fat supplement shake or liquid preparations containing these artificial sweeteners to make them palatable. If you have spoken to any bariatrician, they will tell you, the best way to follow a ketogenic diet is to eat real food. If you want to read about the anecdotal GI effects of sweeteners, read the comment section in Amazon about the Haribo Sugar Free Gummy Bears.

Oh, by the way, 65% of patients in my practice following ketogenic diet see improvement in gastroesophageal reflux (GERD) symptoms. (Austin GL, Thiny MT, Westman EC, Yancy WS Jr, Shaheen NJ. A very low carbohydrate diet improves gastroesophageal reflux and its symptoms: a pilot study. Dig Dis Sci 2006;51:1307–2.)

Hair Loss/Thinning – Really?! It is important to note that hair loss/thinning can occur with any form of weight loss (Novak MA, Meyer JS. Alopecia: Possible Causes and Treatments, Particularly in Captive Nonhuman Primates. Comparative Medicine. 2009;59(1):18-26.) This is especially true if you are restricting calories, which was occurring in a number of the ketogenic dietary studies previously published. You do not and should not need to “restrict calories” if you are following a ketogenic diet correctly, and in fact, most people take in more than 1800 calories on a ketogenic diet. (Shai I, et al., N Engl J Med, 2008; 359:229-241.)

Inflammation Risk – In every patient that I have placed on a ketogenic diet in the last 8 years, all inflammatory markers including CRP, Sedimentation Rate and Uric Acid have all decreased. Inflammation gets better on an appropriately formulated ketogenic diet. The older studies of ketogenic diets in children contain most of their fat from Omega-6 fatty acids from vegetable oil which will increase inflammation and oxidative stress, spike the cortisol levels and have the secondary effect of actually raising the triglycerides. (Simopoulos AP,The importance of the ratio of omega-6/omega-3 essential fatty acids, Biomed Pharmacother., 2002 Oct;56(8):365-79.)

Kidney Stones/Gout – These (Kidney Stones & Gout) are both commonly caused by spikes in uric acid. As noted above, I’ve seen multiple cases in my practice where a ketogenic diet lowers uric acid. Only a small clinical trial has been published in the literature (and it wasn’t truely ketogenic), but the results point to the potential for ketogenic diets to lower uric acid. (Dessein PH, Shipton EA, Stanwix AE, et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis 2000; 59:539-543.) Ketogenic diets also have the capacity to lower the formation of calcium oxalate stones through a secondary mechanism I won’t go into here. Are these a risk? Only if you cheat on your carbohydrate restriction. So, I warn patients. Don’t cheat.

Muscle Cramps/Weakness – The process of weight loss occurs by burning fat into CO₂ and water. We breathe the CO₂out, but the water produced has to follow salts out through the kidneys. Hence, we lose salts. This can cause weakness and muscle cramps. The solution? Stop restricting salt on a low carbohydrate diet. We are the only mammal that restricts salt and we do it because low-fat diets cause us to retain water. Low carbohydrate diets do the opposite. Use sea salt or sip beef or chicken bouillon broth with your dinner. The use of yellow mustard also helps (the small amount of quinine in yellow mustard stops the cramping). If you have congestive heart failure, talk to your doctor about monitoring your salt intake in balance with your diuretic or water pill.

Hypoglycemia – If you read the ketogenic diet research, most of it was done on epileptic children. The diets called for a period of starvation, then the use of a ketogenic liquid based on the John’s Hopkin’s protocol. It is a well-known fact in medicine that starvation in children can frequently cause hypoglycemia, especially in children with other genetic or congenital defects leading to forms of epilepsy. In clinical practice, with ketogenic diet use in adults, hypoglycemia is rare.

Low Platelet Count (Thrombocytopenia) – Again, this was seen in the epileptic children who were placed into starvation first, then introduced a liquid fat replacement shake to stop intractable seizures. These liquids or shakes were often nutrient deficient in other essentials. Folic acid, B12 and copper deficiency can occur when not eating “real food.” Low platelet counts are rarely seen on ketogenic diets based around “real food.” Many children in the ketogenic studies had been on or were concomitantly on valproic acid for their seizures. Valproic acid is commonly known to cause thrombocytopenia (Barry-Kravis E et al, Bruising and the ketogenic diet: evidence for diet-induced changes in platelet function. Ann Neurol. 2001 Jan;49(1):98-103.; Kraut E, Easy Bruising, http://www.uptodate.com, May 2015.)

Impaired Concentration/Mood – A number of patients starting carbohydrate restriction will go through 2-4 weeks of carbohydrate withdrawal. This can be just as powerful as morphine withdrawal in some patients. Sugar is a drug and effects the same hedonic receptors that morphine does in the brain (Lustig, Robert H, Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanon, Journal of the American Dietetic Association , Volume 110 , Issue 9 , 1307 – 1321.) Some patients will experience headache, tremor and decreased concentration while “withdrawing” off of starches and carbohydrates. Studies actually show that after a period of adaptation, cognitive function actually improves (Krikorian R, Shidler MD, Dangelo K, Couch SC, Benoit SC, Clegg DJ. Dietary ketosis enhances memory in mild cognitive impairment. Neurobiology of aging. 2012;33(2):425.e19-425.e27. doi:10.1016/j.neurobiolaging.2010.10.006.)

Metabolic Acidosis – As described above, this can occur in a type I diabetic, and metabolic acidosis has also been shown to occur in young children placed on severe carbohydrate and protein restriction, as was the case in some of the ketogenic dietary trials with epileptic patients. (Saxena VS, Nadkarni VV. Nonpharmacological treatment of epilepsy. Annals of Indian Academy of Neurology. 2011;14(3):148-152. doi:10.4103/0972-2327.85870.; Freeman, et al., The Ketogenic Diet: One Decade Later, Pediatrics March 2007; 119:3 535–543)

Osteoporosis/Osteopenia – If your ketogenic diet is “shake” or “meal replacement” based, you run the risk of mineral deficiency that could lead to Osteoporosis, however, if you are using real food, the opposite is true and most patients have improvement in their Vitamin D levels and bone density. (AG Christina Bergqvist, Joan I Schall, Virginia A Stallings, Babette S Zemel, Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic dietAm J Clin Nutr December 2008 88: 1678–1684; doi:10.3945/ajcn.2008.26099)

Infections/Sepsis/Pneumonia – These have not been issues in the 8 years I have been using ketogenic diets with my patients. These issues were seen in the John’s Hopkins protocol with children who had epilepsy and other congenital disorders placed on a diet low in protein and carbohydrate. (Saxena VS, Nadkarni VV. Nonpharmacological treatment of epilepsy. Annals of Indian Academy of Neurology. 2011;14(3):148-152. doi:10.4103/0972-2327.85870.)

Three year weight loss and metabolic improvement in a patient on a Low-Carb / Ketogenic diet. Note: Patient admits to not following ketogenic diet during holidays from Nov 2013 – Feb 2014 (see the dramatic changes to the body when cheating happens)

Lipid/Cholesterol Changes – In the 8 years I have been applying ketogenic diets to patients, I have seen dramatic improvement in the triglycerides and HDL levels. The only time triglycerides rise over 100 is if the patient is using artificial sweeteners or is cheating on the carbohydrate restriction. Total cholesterol commonly rises, however, this is indicative of the fact that there is a shift in the LDL particle size and this affects the calculation of both total cholesterol and LDL-C. In light of this, most of my patients have dramatic improvement in triglycerides and small dense LDL particle number. I’ve included the common cholesterol changes I seen in my office as a few case reports to demonstrate the effectiveness of a ketogenic diet:

2 year ketogenic dietary labs and weight loss

Myocardial Infarction – It is interesting that one blogger includes this on the list of adverse reactions, however, when you actually read the study, the author of the paper make an “assumption” that there was potential for heart attack due to an elevated total cholesterol, however, a correlation was never made. Again, in the 8 years I have been using ketogenic diets, I have seen dramatic improvement in cholesterol profiles, inflammatory markers, atherosclerosis and carotid intimal studies (Shai I et al, Circulation 2010; 121:1200-1208).

Three year metabolic history of a Low-Carbohydrate / Ketogenic diet

Menstrual Irregularities / Amenorrhea – It is well known that any diet causing protein or other nutritional deficiency will affect the menstrual cycle first and growth second. The only time menstrual irregularities occur with a ketogenic or Low-Carb diet is when a patient is not taking in enough protein or is not eating real food. What amazes me is that a properly applied ketogenic diet causes normalization of the menstrual cycle, and in my practice, I’ve had a number of women successfully be able to conceive after making a ketogenic dietary change.

Death – All cases of death related to ketogenic diets have been documented in children while using liquid formulas for ketosis to treat epilepsy. These cases revealed the formation of a prolonged QT interval leading to cardiomyopathy due to deficiency in selenium. This has been solved by the addition of selenium to the ketogenic supplement. (Stewart WA et al., Acute pancreatitis causing death in a child on the ketogenic diet, J Child Neurol. 2001 Sep;16(9):682.; Bergqvist AG et al, Selenium deficiency associated with cardiomyopathy: A complication of the ketogenic diet. Epilepsia. 2003 Apr;44(4):618-20.; Kang HC et al., Early and lat onset complications of the ketogenic diet for intractable epilepsy, Epilepsia. 2004 Sep;45(9):1116-23.; Kang HC et al, Efficacy and Safety of the Ketogenic diet for intractable childhood epilepsy: Korean Multicentric Experience, Epilepsia. 2005 Feb;46(2):272-9.) This does not happen when the diet is based on the use of real food instead of supplementation and has not been seen in adults.

For more details on the nutrient content of a ketogenic diet, see the recent article by a friend of mine, Maria Emmerich. She’s been creating ketogenic diets for years and has a number of fantastic books my wife and I have been using in our home over the last nine years. She is one among many that can give you some direction on how to devise a healthy, real food based ketogenic diet. See the page on my website here that will give you some direction in formulating your Ketogenic Lifestyle.

Nally Family Low-Carb / Ketogenic Cheese Cake

So, to celebrate Mother’s Day, today, with my family, I am going to indulge in some Low-Carb / Ketogenic Cheese Cake!! Happy Mother’s Day, to all of you and especially to all you mothers out there making a healthy difference in the lives of your families! (You can find the recipe for this delicious cheese cake here)

In the words of Sir William Ostler, “If it were not for the great variability among individuals, medicine might well be a science and not an art.”

June 2, 2014

Inflammation Killer – A Ketogenic Diet

Symptoms of Inflammation seen in Diabetes Mellitus

A recent study published in the Annals of Internal Medicine demonstrate significant improvement in overall inflammation in type II diabetic patients following a carbohydrate restricted diet versus a low fat calorie restricted diet. Another bit of proof demonstrating what I’ve been seeing in my office over the last 8 years. The study reveals significant improvement in glycemic (blood sugar) control in those following a low carbohydrate diet as well as significant lowering of C-reactive protein, IL-1 and IL-6 over those following a low fat diet. You can see the study here.