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.
So, you’ve started a ketogenic lifestyle and you’re a few months in . . . but, is it really working? How do you know? You should be seeing your waist shrink. But, is all that butter really good for my cholesterol? What about my blood tests?
I commonly get these questions over the last 12-13 years of using a low-carbohydrate or ketogenic lifestyle approach in the treatment of obesity, diabetes, cholesterol and high blood pressure. We can determine the effectiveness of the diet on your metabolism with some simple blood testing.
What Lab Tests Do You Need?
Watch the video below to find out what tests are right for you:
Why don’t you check all the other inflammatory markers like HS-CRP, Lp(a), etc? Because, I know that these test will be elevated if insulin is > 5 mmol/L and if sdLDL particle is > 500 nmol/L.
Check out our membership site and the benefits that come with it.
“Won’t my cholesterol get worse and increase my risk of heart disease if I eat more fat?”
I get asked this question at least 3-4 times a day. The answer is, “NO. Not if you cut out the sugar and starch.”
“But, wait?! What about my heart? All that fat can’t be good for my heart?” they ask.
Cholesterol Defined
Let’s start with the contents of the standard cholesterol panel or “Lipid Panel.”
For the last 20-30 years the following labs have been looked at as the holy grail of heart disease risk:
Total Cholesterol
HDL (the measured number for “good” cholesterol)
LDL-C (the calculated number for “bad” cholesterol).
VLDL-C (the calculated number for very low density 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 a steroid precursor that either makes up a part of the lipoprotein molecule or is transported with the triglycerides as a passenger. The lipoproteins are just transporters made of lipid that are only slightly different from their passenger load (causing increased or decreased density). The proteins that are contained within the wall of the lipoprotein transporter is what makes them different. These lipoprotein particles can be thought of, simplistically as buses, carrying triglyceride passengers. Here size does matter, and size determines the function of the molecule at that moment in time.
Cholesterol is Really Just a Triglyceride Bus
These buses, big and small, carry the passengers up and down the vascular system of the body. Glucose can float freely through the blood stream, but the other form of fuel, triglyceride, must be transported via the “lipoprotein bus”. The triglyceride and cholesterol are actually the passengers inside the bus. But triglyceride presence in the system seems to change the density of the lipoproteins. So now picture big, medium and small buses . . . the high density lipoprotein (HDL), intermediate density lipoprotein (IDL) and the low density lipoprotein (LDL) buses.
Triglyceride Changes the Density of Cholesterol
The density of the bus gets lower as triglyceride levels rise and fewer cholesterol esters and proteins are bound. As HDL goes up, LDL-C goes down (Parker TS et al, Proc Natl Acad Sci USA, Feb 1986)
The second problem is the VLDL-C and LDL-C are actually calculated numbers and don’t actually reflect the true presence of the lipoprotein particles as the triglyceride number rises. For the accountants, mathematicians and engineers reading this that calculation is called the Friedwald Equation and is as follows:
This equation falls apart when the triglyceride level is greater than 400 mg/dL (4.52 mmol/L) or patients with hyperinsulinemia.
Total Cholesterol is the sum of the HDL, LDL, as well as intermediate density lipoprotein (IDL) & very low density lipoprotein (VLDL) which aren’t reported in the “Lipid Panel” above. So, total cholesterol is basically the sum of all the buses you have driving around.
The third key piece of information that the Lipid Panel above doesn’t tell you is the lipoprotein categories (HDL, LDL, IDL, and VLDL) are actually have three to four sub-types or sub-particles that are further differentiated by weight and size.
Image Credit: Berkley Heart Labs, Inc.
Improvement in cardiovascular risk, including improvement in cholesterol, inflammation and plaque formation have been the case with every patient I have used a high fat, low carbohydrate (ketogenic) dietary approach with over the last 12 years.
I’ve had so many people ask me how this works, and then, how to explain the changes to their primary doctors or cardiologist, I decided to write the following article. My intent is not to point the finger where others are wrong; but to identify how we, myself included, took a misstep along the path of scientific discovery. This misstep led to guidelines that, for over 45 years, have been accepted by medical students and clinicians as the “gospel truth.”
History of Cholesterol Measurement
The measurement of cholesterol, specifically total cholesterol, started in the 1950’s. There appeared to be a mild correlation of heart disease in countries who’s diets had higher fat intake. Ansel Key’s identified this apparent correlation in his Diet-Heart Hypothesis published in JAMA in 1957. He stated from his observational work that “the results of a fatty diet are hypercholesterolemia [elevated cholesterol].” A number of studies at the time showed that increasing fat intake in the standard diet increased total cholesterol; however, NO LINK to heart disease was ever proven (Ahrens EH, Jr, Lancet, May 1985).
Studies published by E. H. Ahrens, Jr. demonstrated that the cholesterol increased because of carbohydrate intake, not fat alone (Ahrens EH Jr, et al., Trans Assoc Am Physicians, 1961). The actual question, “Does increasing fat alone cause heart disease?” was never answered. The question, as well as known evidence based cholesterol reducing dietary approaches, were ignored in 1984 by the National Institutes of Health (NIH) Consensus Development Conference on Lowering Cholesterol to Prevent Heart Disease that was based heavily on epidemiological data rather than clinical reproducible science (Ahrens EH, Jr, Lancet May 1985).
Despite significant scientific evidence refuting the Diet-Heart Hypothesis, the 1984 NIH decision reflected politics and massive publicity campaigns.
Stop Demonizing My Eggs!
Since 1984, fat and cholesterol containing foods are treated like witches of Salem. As an example, eggs, specifically the egg yolk. (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.
You can’t extrapolate mortality risk based on a single small study that doesn’t actually identify correlation or causation. But the AHA did exactly that in 1961, and they are trying to do it again today. The MR-FIT study, largest study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol. In fact, the Director of the study, Dr. William Castelli actually stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”
“We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least, and were the most physically active,” he said.
Diet-Heart Hypothesis Doesn’t Explain the French Paradox
To add to cholesterol confusion, the Diet-Heart Hypothesis does not explain the “European or French Paradox.” The French prefer cooking in butter instead of vegetable oil. In fact, the French eat 40% fat in their diet. And, more than 15% of that is saturated fat.
The French Paradox
Interestingly, the French and those that eat the most cheese, butter and whole eggs have the lowest rate of coronary vessel calcification and heart disease. Attempts to explain this away as epidemiological error or diet complexities have been published, but still never answers the underlying question, “Does increasing fat alone cause heart disease?” (Ferrieres J, Heart, Jan 2004).
According to the Diet-Heart Hypothesis, people with familial hypercholesterolemia should have much shorter lifespans and are at increased risk of early mortality or death. However, there is actually no scientific evidence of this. In fact, the Honolulu Heart Program study revealed that people with low cholesterol are the ones at significant risk of early mortality or death (Schwartz I, et al., Lancet 2001 Aug). Additionally, higher LDL-C is actually predictive of longer life and has been demonstrated to correlate with longevity (Ravnskov U et al., BMJ Open, 2016 Jun 12;6(6): e010401).
Saturated Fat Isn’t Bad
I hate to burst your bubble, but saturated fat is NOT linked to vascular disease, diabetes or increased mortality (de Souza RJ et al., BMJ 2015,351:h3978).
It is commonly understood that LDL-C will rise as you eat more saturated fat. This is normal on a ketogenic diet. It has been reported in the scientific literature for over twenty years. It is to be expected, because LDL-C is really a measurement of three different LDL sub-particles (“big fluffy, medium, and small dense”). Increased saturated fat intake, while at the same time lowering carbohydrate intake, actually causes a shift in these low density particles to a bigger “fluffier” particle conformation (Griffin BA et al., Clin Sci (Lond), 1999 Sep). We know that the small dense LDL particles are the atherogenic / inflammatory particles participating in the formation of vascular disease and directly correlate with triglyceride levels. We also know the big “fluffy” LDL particles actually reduce the risk of vascular disease (Griffin BA et al., Clin Sci (Lond), 1999 Sep).
Why Do Physicians Still Prescribe STATIN Medications?
So why have clinicians been pushing the use of STATIN medications to reduce risk of coronary heart disease? It started with the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT). This was a study of over 3800 men treated with cholestyramine, a cholesterol lowering medication (JAMA, 1984 Jan. 20;251(3):351-64.). There was a very slight “absolute reduction” in coronary heart disease risk, 1.6% to be exact. LDL-C decreased, but there was no reduction in the risk of death. In fact, there was actually an increase in risk of all cause mortality in the cholestyramine group which was never emphasized.
Overall, cholestyramine reduced non-fatal heart attacks in 60 of the 3,806 men. In other words, one in 63 men improved with the use of this medication . . . not very impressive. However, statistics look more impressive expressed in terms of “relative risk.” Relative risk is the percent increase of those with no treatment from those with treatment. This is always a bigger number.
When the LRC-CPPT researchers calculated relative risk, the percent change between the treated and non-treated was 19%. This bigger number was reported as the “risk reduction.” For those that don’t know the difference between actual risk and relative risk, 19% sounds very impressive! (JAMA. 1984 Jan 20;251(3):351-64.)
False Evidence Emphasized By Relative Risk
This relative risk reduction drove the STATIN era we are well aware of today. Lipitor (atorvastatin) reduces heart disease risk by only 1%. However, when you use the term “relative risk reduction,” it has more psychological effect. Relative risk of 36% sells more drugs.
Crestor (rosuvastatin) was show to have an absolute risk reduction in heart disease by 1.2%. When run through the relative risk reduction statistic it has a claim of 44% relative risk reduction.
These big numbers emphasized false evidences in many clinician’s minds that reducing LDL-C must be really effectively reducing heart disease.
Knowing that the LDL-C doesn’t really give you a clear idea of heart disease risk. It becomes essential to know which type of LDL lipoprotein particle is the atherogenic or heart disease causing particle. Research now points to the small-dense LDL particle as the atherogenic molecule (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr). Studies have identified that elevated small-dense LDL cholesterol correlates much more closely with risk for inflammation, heart disease and vascular disease (Williams PT, et al. Atherosclerosis. 2014 April; 233(2): 713-720.)
A Better Marker for Heart Disease Risk?
Recent research demonstrates that small dense LDL cholesterol is a better marker for prediction of cardiovascular disease than total LDL-C (Hoogeveen RC et al., Arterioscler Thromb Vasc Biol. May 2014, 34(5): 1069-1077l; Ivanova EA et al., Oxidative Med Cell Longev. 2017).
The 2015 British Medical Journal, referenced above, analyzed the relevant 19 peer reviewed medical articles that included over 68,000 participants. This review showed that there is no association of high LDL-C with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart or vascular disease).
In stark opposition to the landmark evidences above, the American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation. I am well aware of their position. They claim that saturated fat is the cause of increased LDL-C. Further, they extrapolate that elevated LDL-C is associated with increase in cardiovascular disease death. This boldfaced claim is based on one single small four-year (2009-2013) literature review completed by the World Health Organization. It looked at very small studies lasting only 3-5 weeks and comprised in total only 2353 participants. That’s not nearly long enough to see fully effective cholesterol changes. And, none of the studies had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).
Clinical Evidence Is Pointing to Ketogenic Lifestyles as a Key
In my office, I see up to 10% regression in carotid stenosis (blockage in the carotid arteries) each year when following a ketogenic dietary lifestyle. Evidence points out that higher fat intake and lowering of carbohydrate intake has a regression effect on plaque and thickness of the arterial wall. (Shai I et al., Circulation, Mar 2010.) And, increased small dense LDL cholesterol correlates with thickening of the carotid arterial wall (Gentile M et al., Clinica Chimica Acta,Naples, Italy Division of Cardiology, Nov 2013, DOI: 10.1016 / j.cca.2013.08.010)
Based on the large body of evidence that sits before us today, the use of total cholesterol and LDL-C to determine vascular disease risk are obsolete and ineffective tools. That’s why we focus on insulin, triglycerides and small dense LDL particles.
Are you worried about your cholesterol?
Is a ketogenic lifestyle right for you?
These are great questions that I hope I can answer. Check out this month’s Kickstart program if you’re just getting started. Or, click here to work with me individually on your ketogenic lifestyle and cholesterol.
What laboratory testing is necessary when you start your weight loss journey on a Ketogenic, Low-Carbohydrate, Paleolithic or any other dietary changes? Why do you need them and what are you looking for? We discuss these questions and others on today’s PeriScope. Lots of questions from around the world to day . . . this one lasted a bit longer than normal . . . 45 minutes to be specific. But it’s a good one because of all of your fantastic questions! You really don’t want to miss this one.
You can see the video below or watch the video combined with the rolling comments here on Katch.me/docmuscles.
A list of the labs that we discussed are listed below:
Fasting insulin with 100 gram 2 or 3 hour glucose tolerance test with insulin assay every hour
CMP
CBC
HbA1c
Leptin
Adiponectin
C-Peptid
NMR Liprofile or Cardio IQ test
Lipid Panel
Urinalysis
Microalbumin
Apo B
C-reactive protein
TSH
Thyroid panel
Thyroid antibodies
AM Cortisol
This list will at least get one started, provide the screening necessary to identify insulin resistance (Diabetes In-Situ), Impaired fasting glucose, diabetes and allow for screening for a number of the less common causes of obesity.
I would highly recommend that you get these through your physician’s office so that appropriate follow up can be completed. These labs will need to be interpreted by your physician, someone who understands and is familiar with various causes of obesity.
Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.
First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)
However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).
There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).
Weight & Size of VLDL, LDL & HDL
Why LDL-C is misleading: Identical LDL-C of 130 mg/dL can have a low risk (Pattern A) with a few “big fluffy LDL particles or high risk (Pattern B) with many small dense LDL particles.
Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.
Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.
Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).
Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.
I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:
Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
Shai I et al. Cirulation. 2010; 121:1200-1208
Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy
This week I had the pleasure of seeing a really nice 46 year old Hispanic male who is fairly new to the office. He came back in to see me in follow up on his diabetes. To give you a bit of background history, the patient came to see me about 6 months ago, just not feeling very well. Based on his symptoms of fatigue, history of elevated blood sugar and family history, lab work was completed.He saw us initially with a Hemoglobin A1c of 12.3% in June (normal should be 4.9%-5.6%). This means he had an average blood sugar over the previous three months of about 310 mg/dL (normal should be < 110 mg/dL).
Past Medical History include: Diabetes Mellitus – type II (not on any medications when initially seen), Hypertension (high blood pressure), Dyslipidemia (elevated cholesterol) and a non-specific heart arrhythmia.
Medications: None
Surgeries: Knee & shoulder arthroscopies
Family History: Father Diabetes, Stroke, Heart Disease, Hypertension, Elevated Cholesterol
After getting his labs back, we had a very long conversation about the need to either fix his diet dramatically, or he may be looking at using 3-4 oral medications or even insulin to control his blood sugar.
When I see average blood sugars (HbA1c) stay over 6.5% (or greater than 140 mg/dL), the risk for retinal, kidney and nerve damage is significant and often irreversible after 4-5 years. Most physican’s are affraid to lower the HbA1c to less than 7.0% with medications due to low blood sugar events, and so the diabetes community has “settled” with 7.0% as being effective. However, it still isn’t low enough. I saw this happen with my father and with other members of me family. I’ve seen it happen over and over with my patients over the last 15 years when they have not lowered their blood sugar and reduced the high insulin loads that occur in response to those high blood sugar levels. It has been my experience that HbA1c can be very safely lowered to the normal range, as low as 5.2-5.6% without symptomatic low blood sugars, with the correct diet and careful use of medications.
As you can see, a dramatic change in his blood sugar has occurred in a three month interval. Not only that, we see a significant change in his cholesterol profile.
Previously, we looked at LDL-C for heart disease risk, however, I have multiple patients that have had heart disease with normal LDL-C ( <100 mg/dL). LDL-C is just a summation of all the particles. The LDL particle is actually made up of three sub-types and it is specifically the small dense particle that causes the vascular risk. You can see a dramatic normalization of the small dense particle LDL with no change in LDL-C and minimal change in Total Cholesterol in the patient’s labs when he reduces his carbohydrate intake. This is a pattern I see every single day. When serial carotid ultrasound studies are completed, I see reduction in blockage and reduction in the vascular wall thickening. I will be very interested to see the vascular studies on this patient and I will await his results as he tightens up his diet even further.
All in all, he has dramatically brought his diabetes under control with carbohydrate restriction and if he continues this lifestyle, he has reduced his risk for retinal damage, reduced his risk for kidney damage, reduced his risk for nerve damage and essentially added 20 years to his life.
(Disclosures: Dr. Nally has no vested interest, monitary or otherwise, in Novo Nordisc or it’s products including liraglutide.)
