Statin drugs have been show to increase risk of death with a COVID-19 infection.
Tag: Cholesterol
Just Keep Esterifying
I’ve had many of my patients and followers on social media ask about my continued use of the hashtag #JustKeepEsterifying. Well, here is the answer. Check out the short 4 minute video below to get the answer:
All About Fat on a Ketogenic Diet (Can You Eat Too Much Fat?)
Catch my new video. I go into depth regarding why the type of fat you eat is very important on a ketogenic lifestyle. I reviews the effects of short, medium and long chain fats and how they are absorbed and used. We talk about starting a ketogenic diet and answer multiple viewer questions. Check it out!
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.
The Conundrum of Cholesterol & Ketones
Watch as Dr. Nally discusses how eating more fat actually lowers your cholesterol and your risk for heart disease. Is a ketogenic lifestyle more effective than cholesterol medication? Find out as we discuss this an many fascinating cholesterol questions from Dr. Nally’s Periscope watchers from around the world. He also answers questions about his KetoEssentials Multi-Vitamin, Exogenous Ketones, and Pork Rinds (his favorite are the Pork Clouds brand).
So, mix up a bowel of fluff and grab a spoon while you listen and lower your cholesterol.
KetoTalk From the Caribbean Sea
Dr. Nally recently spoke about Low-Carbohydrate/Ketogenic Diets on the 2016 Low Carb Cruise to the Eastern Caribbean. While there, he and Jimmy Moore recorded another episode of KetoTalk with Jimmy and the Doc.
Listen in to KetoTalk Episode 20: A LIVE Q&A Session From The 2016 Low-Carb Cruise
Here’s what Jimmy and Dr. Nally talked about in Episode 20:
– We are in front of a LIVE audience of Ketonians
– How long will you experience hair loss when you go ketogenic?
– What role does resistant starch have on the keto diet?
– Is eating high-fat with high-carb harming my boyfriend?
– How does intermittent fasting help with keto?
– Whether to count total vs. net carbohydrates
– Whether you need to cycle carbs when building muscle
– What the best way to test your ketones is
– How to test blood ketones on a budget
– What the difference is between an NMR and basic lipid panel
– The dramatic changes in your cholesterol when going keto
– How long should you be on keto before running blood tests?
– Whether you should cut fat lower on keto to speed up weight loss
– Is having a lower body temperature a bad thing when eating keto?
You can listen at the iTunes page here, or download it for free to your favorite iTunes player.
Ketogenic Lifestyle Rule #3: Be BOLD or Be Italic, but never be Regular: Why Size Matters with Cholesterol
On this evenings PeriScope video we talked about cholesterol. And, and you can see an updated, in depth discussion about cholesterol on my YouTube channel here. Please go check it out and if you find it helpful, please follow me here and on YouTube. The is the burning question on everyone’s mind who starts a Low-Carb, High Fat or Ketogenic Diet: “What will happen to my cholesterol if I lower my carbohydrates and eat more fat?”
The answer . . . it will improve!
How do I know this? I’m an obesity specialist. I specialize in FAT or lipids (to put it kinder scientific terms). To specialize in fat, one must know where it came from, what it’s made of and where it is going. And, this has been the case with every single patient I have used this dietary change with for the last ten years, myself included.
Lets start with the contents of the standard cholesterol or “Lipid Panel”:
- Total Cholesterol
- HDL-C (the calculated number for “good” cholesterol)
- LDL-C (the calculated number for “bad” cholesterol).
- Triglycerides
The first problem with this panel is that it makes you believe that there are four different forms of cholesterol. NOT TRUE! Actually cholesterol is cholesterol, but it comes in different sizes based on what it’s function is at that moment in time. Think of cholesterol as a bus. There are bigger busses and smaller busses. Second, triglyceride is actually the passenger inside the HDL and the LDL busses. And third, Total Cholesterol is the sum of the HDL, LDL, as well as ILDL & VLDL which aren’t reported in the “Lipid Panel” above.
The fourth thing that this panel doesn’t tell you is that HDL & LDL are actually made up of sub-types or sub-particles and are further differentiated by weight and size.
For our conversation, we need to know that the number of LDL particles (LDL-P) can actually be measured in four different ways and these measurements have identifed that there are three sub-types: “Big fluffy” large dense LDL, medium dense LDL, and small-dense LDL. Research has identified that increased numbers of small-dense LDL correlates closely with risk for inflammation, heart disease and vascular disease (1).
If you’ve been a follower of my blog for a while, you’ve seen this picture before. This picture illustrates why an LDL-C (the bad cholesterol measurement) can be misleading. Both sides of the scale reflect an LDL-C of 130 mg./dl. However, the LEFT side is made up of only a few large fluffy LDL particles (this is the person with reduced risk for heart disease) called Pattern A or a LDL healthy cholesterol level. Even though the LDL-C is elevate above the recommended level of 100 mg/dl, the patient on the left has much less risk for vascular disease (this is why you CAN’T trust LDL-C as a risk factor).
The RIGHT side of the scale shows that the same 130 mg/dl of LDL-C is made up of man more small dense LDL particles (called “sd LDL-P”) with a Pattern B type that is as increased risk for heart or vascular disease. This is where the standard Lipid Panel above, fails to identify heart disease and it’s progression.
Research tells us that the small dense LDL particle levels increase as the triglycerides increase. And we know that Triglyceride levels increase in the presence of higher levels of insulin leading to a cascade of inflammatory changes. Insulin is directly increased by the ingestion of simple and complex carbohydrates. Insulin also increases with the ingestion of too much protein. So, that chicken salad or the oatmeal you ate, thinking it was good for you, actually just raised your cholesterol. If you are insulin resistant, your cholesterol just increased by 2-10 times the normal level (see my article here on how insulin resistance causes this.)
“Ok, but Dr. Nally, there are four different companies out in the market measuring these fractional forms of cholesterol. Which one should I choose?”
There are actually five different ways you can check your risk.
- Apolipoprotein levels. This can be done through most labs; however, this test doesn’t give you additional information on insulin resistance that the other tests can.
- Berkley Heart Lab’s Gradient Gel Electrophoresis – This test gives a differentiation based on particle estimation between Pattern A and Pattern B
- Vertical Auto Profile (VAP-II) test by Arthrotec – This test determines predominant LDL size but does not give a quantifiable lipoprotein particle number which I find very useful in monitoring progression of insulin resistance and inflammation.
- NMR Spectroscopy from LipoScience – This test measures actual lipoprotein particle number as well as insulin resistance scores and will add the Lp(a) if requested. I find the NMR to be the most user friendly test and useful clinically in monitoring cholesterol, vascular risk, insulin resistance progression and control of the inflammation caused by diabetes. This test has the least variation based on collection methods if frozen storage is used.
- Ion-Mobility from Quest – This test also measures lipoprotein particle number but does not include insulin resistance risk or scoring. Because the test is done through a gas-phase electric differential, the reference ranges for normal are slightly different from the NMR.
In regards to screening for cardiovascular risk, the use of all five approaches are more effective than the standard lipid panel. However, I have found that clinically the NMR Lipo-profile or the Cardio I-Q Ion-Mobility tests are the most useful in additionally monitoring insulin resistance, inflammation, and disease progression.
It is was the use of these tests that demonstrated to me the profound effect of carbohydrate restriction and ketogenic lifestyles on vascular and metabolic risk. We talk more about these tests on my YouTube video .
Hope this helps.
References:
- Williams PT, et al. Comparison of four methods of analysis of lipoprotein particle subfractions for their association with angiographic progression of coronary artery disease. Atherosclerosis. 2014 April; 233(2): 713-720.
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