Statin drugs have been show to increase risk of death with a COVID-19 infection.
Category: 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:
What You MUST Know about Total Cholesterol & LDL-C on a Ketogenic Diet
Is following your Total Cholesterol and LDL-C really that important?
You may be quite surprised.
Watch as we discuss the important markers of heart disease and vascular disease risk. We will talk about how these markers can help you understand what your body is doing in the process of making or reversing atherosclerosis (plaque in the vessels). And, should you really be taking that STATIN (cholesterol lowering) drug? Get the scoop here as Dr. Nally very simply points out how the right diet can and will lower your cholesterol without the use of medications.
Research in the last 10 years points to the small-dense LDL particle as the atherogenic component of cholesterol (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr). Studies in the last five years 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.)
Recent research in the last three years 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).
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). And, a low LDL-C actually increases risk of early mortality (Schwartz I et al., Lancet 2001, 358: 351-55).
It is commonly understood that LDL-C will rise with increased saturated fat intake on a ketogenic diet. This has been know and reported in the scientific literature for over twenty years. This 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).
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). I realize that, in stark opposition to the landmark review above, The American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation. They stated that saturated fat is the cause of increased LDL-C and they further extrapolated that elevated LDL-C is associated with an increase in death by cardiovascular disease. This boldfaced claim is only based on one single small four year (2009-2013) literature review completed by the World Health Organization with a total of only 2353 participants, most of these studies only lasting 3-5 weeks (not nearly long enough to see fully effective cholesterol changes) and none of which had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).
Based upon the most current scientific evidence above and my clinical experience, the large body of evidence above demonstrates the use of total cholesterol and LDL-C to determine vascular disease risk to be ineffective tools. A low carbohydrate/ketogenic diet lowers small dense LDL cholesterol, triglycerides and blood sugar and in many cases, the use of cholesterol drug (STATIN) therapy is not needed and ineffective in comparison with a ketogenic/carbohydrate restricted lifestyle.
What Blood Tests are Important In a Ketogenic Lifestyle?
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.
The Ketogenic Cholesterol Quandry
“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:
- LDL-C mmol/L = [Tot Cholesterol (mmol/L)] – [HDL-C (mmol/L)] – [TG (mmol/L) / 2.2]
- LDL-C mg/dL = [Tot Cholesterol (mg/dL)] – [HDL-C (mg/dL)] – [TG (mg/dL) / 5]
- VLDL-C = [TG / 5] as a calculated estimate
- 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.
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.
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.
If you want more information about cholesterol and atherosclerosis, please checkout my latest YouTube video on cholesterol and atherosclerosis.
Vascular Plaque Reduction with Ketogenic Diet – A Case Study
Does your diet really reverse vascular disease? I mean, will the diet you’re following ACTUALLY reverse the plaque burden that has occurred over the years of eating the SAD diet (Standard American Diet)?
It appears that the ketogenic diet does. At least that’s what research is showing, and that’s what I am seeing clinically. Let me give you an example. Reversal of vascular disease is what I saw last week in this patient case study in my office.
Meet “Mrs. Plaque” (name has been changed to protect her identity). She is a very pleasant 78 year old female who has been seeing me as a patient for the last 10 years. We identified worsening cholesterol and hyperinsulinemia in this patient a few years ago, and last year, she finally decided to go on a ketogenic diet after we noted slight worsening blood sugar (HbA1c increased to 6.1%), worsening cholesterol and a recent TIA (transient ischemic attack or “mini stroke”). We identified a 44% blockage in her left internal carotid artery and a 21% blockage in the right internal carotid artery putting her at risk for further cerebral ischemic events like a stroke and/or other vascular events like a possible heart attack down the road. She refused STATIN therapy as she had previous myalgia and side effects with their use in the past.
Past Medical History: Hyperlipidemia, Impaired Fasting Glucose (Pre-Diabetes),.Asthma, GERD, Irritable Bowel, Generalized Anxiety, Idiopathic Peripheral Neuropathy, Surgical Menopause (Hysterectomy) with Secondary Atrophic Vaginitis, Recent TIA, Cataracts, Appendectomy
Medications: Plavix 75mg one daily, Premarin Cream 0.635mg every other day, Xanax 0.5mg at bedtime for anxiety, Lyrica 50mg one nightly for neuropathy, Vitamin D 2000 IU daily , TUMS 750mg twice a day.
Her carotid ultrasound and carotid medial intimal thickness (CIMT) study completed April 1, 2015 is present below. You can see that her intimal thickness is only slightly higher than the average female her age, however, she has notable internal carotid artery blockage in both the right and the left sides.
The “mini stroke” and the report above, convinced her that she needed to tighten up her diet. The patient’s husband was also a diabetic and the patient had been “partially” restricting sugar in her diet up to this point in time, however, she had not fully jumped on the ketogenic band wagon. At this point she decided to change her diet.
She was placed on a ketogenic diet, restricting her carbohydrates to no more than 20 grams per day and increasing total fat to >50-60% of her total calories. Nothing else changed including her medications. She followed this program for the next year and this is the blood work that she had while following this program:
4/2/2015 | 8/4/2015 | 11/6/2015 | 5/12/2016 | |
HbA1c (%) | 6.1 | 5.8 | 5.2 | |
Tot Chol (mg/dL) | 224 | 156 | 230 | 233 |
HDL (mg/dL) | 76 | 76 | 87 | 96 |
LDL-C (mg/dL) | 134 | 65 | 128 | 123 |
Small Dense LDL-P (nmol/L) | 481 | 150 | 222 | 217 |
Triglycerides (mg/dL) | 72 | 76 | 74 | 68 |
Fasting Insulin (uIU/mL) | 12 | |||
Glucose (mg/dL) | 91 | 95 | 92 | 85 |
Because she was already partially restricting her sugar intake, her triglycerides and small dense LDL particle number was not bad, however, her average blood sugars were still significantly elevated. Weight decreased from 127 lbs to 119 lbs in August. She admits to slightly increased protein intake over the holidays and her weight increased back up to 125 lbs as of her last visit.
These labs also demonstrate that Total Cholesterol and LDL-C don’t appear to correlate with regression of plaque.
The image below is the patient’s repeat CIMT and carotid ultrasound 13 months later through the same lab. What is dramatic is that she has had over 10% regression in the plaque in both internal carotid arteries and a return of her carotid intimal thickness to the average female in her age bracket.
This case study is consistent with the findings of Dr.Shai and his group when they did a two year comparative dietary intervention study of Low Fat – Group 1, Mediterranean Diet – Group 2, and a Ketogenic Diet – Group 3 on vessel wall volume and CIMT.
Carotid IMT changed by −1.1% from 0.816 mm at baseline to 0.808 mm after 2 years (P=0.18), with no significant difference between diet groups (P=0.91). There was a trend toward significant correlation between the 2-year changes in carotid IMT and VWV (r=0.173, P=0.056).
So, does your diet reverse vascular disease? Evidence is pointing to the fact that the ketogenic diet does. I return to the statement Hippocrates made over 2000 years ago, “Let food be thy medicine, and let medicine be thy food.”
Oh, and pass the bacon.
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.
Diabetes Mellitus – Really the Fourth Stage of Insulin Resistance
I just completed my reading of Dr. Joseph Kraft’s Diabetes Epidemic & You. This text originally printed in 2008 and was re-published in 2011. I am not really sure why I have never seen this book until now, but I could not put it down. I know, I am a real life medical geek. But seriously, you should only read this book if you are concerned about your health in the future. Otherwise, don’t read it.
For the first time in 15 years, someone has published and validated what I have been seeing clinically in my office throughout my career. Dr. Kraft is a pathologist that began measuring both glucose and insulin levels through a three hour glucose tolerance blood test at the University of Illinois, St. Joseph Hospital in Chicago. This test consists of checking blood sugar and insulin in a fasted state, and then drinking a 100 gram glucose load followed by checking blood sugar and insulin at the 30, 60, 120 and 180 minute marks (a total of three hours).
Dr. Kraft completed and recorded this test over a period of almost 30 years on 14,384 patients between 1972 and 1998. His findings are landmark and both confirm and clarify the results that I have seen and suspected for years.
I am convinced that our problem with treating obesity, diabetes and the diseases of civilization has been that we defined diabetes as a “disease” based on a lab value and a threshold instead of identifying the underlying disease process. We have been treating the symptoms of the late stage of a disease that started 15 to 20 years before it is ever actually diagnosed. Diabetes is defined as two fasting BS >126, any random blood sugar >200, or a HbA1c >6.5%. (Interestingly this “disease” has been a moving target. When I graduated from medical school it was two fasting blood sugars >140 and the test called hemoglobin A1c (HbA1c) that we use today for diagnosis didn’t even exist). The semantics associated with this problem is that many of us recognize that the disease is not actually diabetes. The disease is (as far as we understand it today) insulin resistance or hyperinsulinemia. This is where Dr. Kraft’s data is so useful. Diabetes, as it is defined above, is really the fourth stage of insulin resistance progression over a 15-20 year period and Dr. Kraft’s data presents enormous and very clear evidence to that effect.
When I first entered private practice 15 years ago, I noticed a correlation and a very scary trend that patients would present with symptoms including elevated triglycerides, elevated fasting blood sugar, neuropathy, microalbuminuria, gout, kidney stones, polycystic ovarian disease, coronary artery disease and hypertension that were frequently associated with diabetes 5-15 years before I ever made the diagnosis of diabetes mellitus. I began doing 2 hour glucose tolerance tests with insulin levels and was shocked to find that 80-85% of those people were actually diabetic or very near diabetic in their numbers. The problem with a 2 hour glucose tolerance test, is that if you are diabetic or pre-diabetic, you feel miserable due to the very profound insulin spike that occurs. A few patients actually got quite upset with me for ordering the test, both because of how they felt after the test, and the fact that I was the only physician in town ordering it. So, in an attempt to find an easier way, I found that the use of fasting insulin > 5 nU/dl, triglycerides > 100 mg/dl and small dense LDL particle number > 500 correlated quite closely clinically with those patients that had positive glucose tolerance tests in my office. There is absolutely no data in the literature about the use of this triangulation, but I found it to be consistent clinically.
I was ecstatic to see that Dr. Kraft plowed through 30 years and over 14,000 patients with an unpleasant glucose tolerance test and provided the data that many of us have had to clinically triangulate. (I’m a conservative straight white male, but if Dr. Kraft would have been sitting next to me when I finished the book this afternoon, I was so excited that I probably would have kissed him.)
Insulin resistance or hyperinsulinemia (the over production of insulin between 2-10 times the normal amount after eating carbohydrates) is defined as a “syndrome” not a disease. What Dr. Kraft points out so clearly is that huge spikes in insulin occur at 1-2 hours after ingestion of carbohydrates 15-20 years prior to blood sugar levels falling into the “diabetic range.” He also demonstrates, consistently, the pattern that occurs in the normal non-insulin resistant patient and in each stage of insulin resistance progression.
The information extrapolated from Dr. Kraft’s research give the following stages:
From the table above, you can see that the current definition of diabetes is actually the fourth and most prolifically damaging stage of diabetes. From the data gathered in Dr. Kraft’s population, it is apparent that hyperinsulinemia (insulin resistance) is really the underlying disease and that diabetes mellitus type II should be based upon an insulin assay instead of an arbitrary blood sugar number. This would allow us to catch and treat diabetes 10-15 years prior to it’s becoming a problem. In looking at the percentages of these 14,384 patient, Dr. Kraft’s data also implies that 50-85% of people in the US are hyperinsuliemic, or have diabetes mellitus “in-situ” (1). This means that up to 85% of the population in the U.S. is in the early stages of diabetes and is the reason 2050 projections state that 1 in 3 Americans will be diabetic by 2050 (2).
Insulin resistance is a genetically inherited syndrome, and as demonstrated by the data above has a pattern to its progression. It is my professional opinion that this “syndrome” was, and actually is, the protective genetic mechanism that protected groups of people and kept them alive during famine or harsh winter when no other method of food preservation was available. It is most likely what kept the Pima Indians of Arizona, and other similar groups, alive while living for hundreds of years in the arid desert. This syndrome didn’t become an issue among these populations until we introduced them to Bisquick and Beer.
The very fascinating and notably exciting aspect of this whole issue is that insulin resistance is made worse by diet and it is completely treatable with diet. This is where the low carbohydrate diet, and even more effective ketogenic diet or lifestyle becomes the powerful tool available. Simple carbohydrate restriction reverses the insulin spiking and response. In fact, I witness clinical improvement in the insulin resistance in patients in my office over 18-24 months every day. You can get a copy of my Ketogenic Diet here in addition to video based low carbohydrate dietary instruction.
Until we are all on the same page and acknowledge that diabetes is really the fourth stage of progression on the insulin resistance slippery slope, confusion and arguments about treatment approaches will continue to be ineffective in reducing the diseases of civilization.
References:
- Kraft, JR. Diabetes Epidemic & You: Should Everyone Be Tested? Trafford Publishing, 2008, 2011. p 1-124
- Boyle JP et al. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence, http://www.pophealthmetrics.com/content/8/1/29 Accessed November 22, 2015
How Fat Makes You Skinny . . . (Eating Fat Lowers Your Cholesterol?!)
Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.
First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)
However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).
There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).
Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.
Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.
Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).
Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.
I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:
https://www.katch.me/docmuscles/v/2f0b6d07-d56a-368b-b4f6-34a5ab3da916
Or, you can watch the video below:
References:
- Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
- Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
- Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
- Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
- Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
- Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
- Shai I et al. Cirulation. 2010; 121:1200-1208
- Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
- Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy
Reversal of Diabetes in the Ketogenic Zone – A Case Report
This week I had the pleasure of seeing a really nice 46 year old Hispanic male who is fairly new to the office. He came back in to see me in follow up on his diabetes. To give you a bit of background history, the patient came to see me about 6 months ago, just not feeling very well. Based on his symptoms of fatigue, history of elevated blood sugar and family history, lab work was completed.He saw us initially with a Hemoglobin A1c of 12.3% in June (normal should be 4.9%-5.6%). This means he had an average blood sugar over the previous three months of about 310 mg/dL (normal should be < 110 mg/dL).
Past Medical History include: Diabetes Mellitus – type II (not on any medications when initially seen), Hypertension (high blood pressure), Dyslipidemia (elevated cholesterol) and a non-specific heart arrhythmia.
Medications: None
Surgeries: Knee & shoulder arthroscopies
Family History: Father Diabetes, Stroke, Heart Disease, Hypertension, Elevated Cholesterol
Social History: Non-Smoker, Limited Alcohol Use
He related to me that he had been on metformin before, however, had some significant diarrhea and was not interested in using this medication EVER again. A previous doctor had tried Victoza© (liraglutide), a GLP-1 inhibitor, but he didn’t use it for very long as he didn’t really see much change with this medication.
After getting his labs back, we had a very long conversation about the need to either fix his diet dramatically, or he may be looking at using 3-4 oral medications or even insulin to control his blood sugar.
When I see average blood sugars (HbA1c) stay over 6.5% (or greater than 140 mg/dL), the risk for retinal, kidney and nerve damage is significant and often irreversible after 4-5 years. Most physican’s are affraid to lower the HbA1c to less than 7.0% with medications due to low blood sugar events, and so the diabetes community has “settled” with 7.0% as being effective. However, it still isn’t low enough. I saw this happen with my father and with other members of me family. I’ve seen it happen over and over with my patients over the last 15 years when they have not lowered their blood sugar and reduced the high insulin loads that occur in response to those high blood sugar levels. It has been my experience that HbA1c can be very safely lowered to the normal range, as low as 5.2-5.6% without symptomatic low blood sugars, with the correct diet and careful use of medications.
So, my patient, above, committed to change. I was worried that diet alone would not be able to lower these levels enough to be effective so we discussed tight carbohydrate restriction, the addition of methlyated folate and chromium and a re-trial of a low dose of Victoza© (liraglutide), which he had at home.
I didn’t see him for about three months. When he followed up this week I was amazed. I was amazed because I rarely see more than 1.5% drop in HbA1c with the addition of Victoza© (liraglutide). The additional 4.5% of drop with diet was dramatically impressive.
When we talked, he told me that all he has done differently is use the Victoza© (liraglutide) and cut his carbohydrate intake to less than 10 grams per meal (Yes, he did admit to occasionally cheating).
You can see the dramatic results:
June 2015 |
September 2015 |
|
Glucose |
258 |
103 |
HbA1c |
12.3% |
6.3% |
Urine Creatinine (Random) |
208 |
72 |
|
||
Total Cholesterol (mg/dL) |
219 |
218 |
Triglycerides (mg/dL) |
137 |
117 |
HDL-C (mg/dL) |
38 |
37 |
LDL-C (mg/dL) |
154 |
158 |
LDL-P (nmol/L) |
2172 |
1691 |
Small dense LDL-P (nmol/L) |
1289 |
419 |
|
||
TSH (mU/L) |
1.75 |
|
|
As you can see, a dramatic change in his blood sugar has occurred in a three month interval. Not only that, we see a significant change in his cholesterol profile.
Some might argue that this is the Victoza© (liraglutide) doing this. I can tell you, in the 15 years I’ve been doing this and in the 5 years that Victoza© (liraglutide) has been available in the U.S., I have never seen a drug reduce blood sugar or cholesterol this dramatically.
Previously, we looked at LDL-C for heart disease risk, however, I have multiple patients that have had heart disease with normal LDL-C ( <100 mg/dL). LDL-C is just a summation of all the particles. The LDL particle is actually made up of three sub-types and it is specifically the small dense particle that causes the vascular risk. You can see a dramatic normalization of the small dense particle LDL with no change in LDL-C and minimal change in Total Cholesterol in the patient’s labs when he reduces his carbohydrate intake. This is a pattern I see every single day. When serial carotid ultrasound studies are completed, I see reduction in blockage and reduction in the vascular wall thickening. I will be very interested to see the vascular studies on this patient and I will await his results as he tightens up his diet even further.
All in all, he has dramatically brought his diabetes under control with carbohydrate restriction and if he continues this lifestyle, he has reduced his risk for retinal damage, reduced his risk for kidney damage, reduced his risk for nerve damage and essentially added 20 years to his life.
(Disclosures: Dr. Nally has no vested interest, monitary or otherwise, in Novo Nordisc or it’s products including liraglutide.)
Fructose and High Triglycerides Lead to Leptin Resistance
I can’t help myself. Some days I enjoy a good murder mystery, but on others, I enjoy a good journal article elucidating our understanding of leptin. No, leptin is not a tiny Irish folk character or even a superhero. Leptin is a hormone. It’s made by fat cells. Anything made by fat cells becomes fascinating to a “fat doctor.”
Why is learning about leptin illuminating?
Well, if Sir Arthur Conan Doyle was an Obesity Specialist, the mystery would have been that Mr. Plump was killed by the wrench in the kitchen, but the wrench seems to have never left tool case in the garage. No one has been able to figure out how leptin, the allegorical wrench, plays its roll in lepin resistance. We know that a lack of leptin allows hunger to persist and a person without leptin will continue to eat without the sensation of feeling full – leading to obesity. What we haven’t understood is – what causes the brain to no longer sense larger and larger amounts of leptin being produced by those who are obese.
That is . . . we haven’t understood it until now. . .
We have known for some time that the hormone leptin is a key hormone produced by the adipose (fat) cells that suppresses hunger. A majority of obese patients in my clinic have elevated circulating leptin levels 2-10 times the normal levels. We know that a lack of leptin leads to obesity, but the patients that I see in the office are producing an over abundance consistent with leptin resistance. The leptin signal is not being recognized by the brain. This is very similar to type II diabetes and insulin resistance. The pancreas is producing an over abundance of insulin, but the cells are recognizing the signal to let the glucose in through the door way.
Three recent and very interesting studies have pointed to the probable cause. First, one of the most common genetic disorders causing human obesity is loss of function of the melanocortin receptor.
If the MC-4R receptor is broken, suppression of appetite is limited, continued eating occurs and weight gain continues. Leptin, produced by every adipose cell in the body, is carried in the blood stream to the brain and must pass through the blood-brain barrier. Once it crosses the blood-brain barrier and enters the hypothalamus, it has a stimulatory effect on the MC-3R receptor in the Arcuate Nucleus of the hypothalamus causing stimulation of the MC-4R receptor in the Parventricular Nucleus and Lateral Hypothalamus to turn off hunger.
However, if leptin cannot cross the blood brain barrier, the signal is never received from the adipose cells and continued eating without satiation (feeling full) persists. Studies have shown that dietary fructose ingestion alone or in combination with diets high in fat suppress the transmission of leptin across the blood-brain barrier.
Fructose is the primary component of high-fructose corn syrup, and makes up 45-50% of every other type of natural form of sugar (sucrose). Yes, it’s the major component found in table sugar, brown sugar, honey, agave, molasses and maple syrup. This is why a Paleolithic Diet isn’t fully effective for people with leptin resistance.
Lastly, anything that raises triglycerides inhibits leptin from crossing the blood-brain barrier.
Insulin has a direct effect on triglycerides. (See the articles “Insulin Resistance & The Horse,” “Fat Thoughts on Cholesterol,” “Ketogenic Living” and “So, What is this Ketogenic Thing?“). If your insulin levels go up, triglyceride production goes up. The patient with insulin resistance, pre-diabetes, impaired fasting glucose or type II diabetes produces between two to ten times the normal amount of insulin when eating the standard American diet (SAD diet). These patients have significant triglyceride elevation because of the high insulin response to carbohydrates in their diet. (Many of them were told by their doctor that “It’s just genetic so take your Lipitor.”) Statin drugs lower the LDL-C (calculated “bad cholesterol” level), but don’t reduce triglycerides effectively. Inadequate treatment of high triglycerides allows poor blood-brain barrier transmission of leptin and worsening leptin resistance.
In fact, this is the challenge and problem with the “frequent fasting” or “intermittent fasting” fad for weight loss that has been popping up in the blogosphere. If fasting reaches a state of starvation (which is a very fine line metabolically), it stimulates a stress response . . . causing a spike in cortisol, release of glycogen (a form of sugar), a compensatory release of insulin and a spike in triglycerides. If you have tried intermittent fasting and you’ve gained weight, you are probably not “fasting,” your probably “starving.” We’ve known for years that triglycerides are elevated in starvation. This diminishes leptin’s ability to cross the blood-brain barrier and leads to worsening leptin and insulin resistance.
High leptin levels caused by leptin resistance also seems to play a significant role in the development of diabetic retinopathy – damage to the tiny blood vessels at the back of the eye feeding the retina. Diabetic retinopathy starts insidiously without any symptoms initially and can lead to eventual blindness if not treated. Leptin seems to upregulate vascular endothelial growth factor (VEGF) which leads to narrowing of the blood vessels called “ischemia.” Chronic ischemia of the retinal vessels leads to damage to the delicate retinal cells of the eye.
So what do you do if you have leptin resistance. First, eliminate carbohydrates from your diet, especially sugars, high fructose corn syrup and any other form of simple sugar. This is why I am such a big fan of low carbohydrate, high fat diets.
Second, lower your triglycerides. This is done through decreasing overall insulin loads and is very effectively accomplished with a ketogenic diet. You can find this in my book, The KetoCure. Some additional great sources are KetoClarity, The Art and Science of Low Carbohydrate Living, and The Ketogenic Cookbook.
Third, use a supplement containing alpha-lipoic acid, carnosine high gamma vitamin E and benfothiamin (derivative of Vitamin B1). These have been demonstrated to decrease inflammation and render protection to the blood vessels.
The use of Epigallocatechin gallate (EGCg), a derivative extract of green tea, has been shown to repress hepatic glucose production, one of the insidious factors of insulin resistance, and may play a role in stabilizing the effect insulin has on production of triglycerides. You should consider using KetoEssentials. It is my specially formulated multivitamin that contains all of the above supplements, and includes methylated folic acid (B9), the necessary vitamin B6 & B12, chromium, vandium & zinc that help to further stabilize insulin resistance.
Fourth, get a good night’s sleep. Lack of sleep causes a stress response, increases cortisol, raises blood sugar and insulin leading to further leptin resistance.
Fifth, mild to moderate resistance exercise has been shown for years to improve insulin resistance significantly. If you’re not exercising, take a 20 minute walk 2-3 times per week, ride a bike for 20 minutes, start a weight lifting program, consider yoga or Pilates, Remember, jumping to conclusions, flying off the handle, carrying things too far, dodging responsibility and pushing your luck don’t qualify as resistance exercise.
Above all, if you’re having trouble losing weight, controlling insulin or leptin, see your doctor. He or she can really help.
References:
- Ray F. Gariano, Anjali K. Nath, Donald J. D’Amico, Thomas Lee, and M. Rocio Sierra–Honigmann. “Elevation of Vitreous Leptin in Diabetic Retinopathy and Retinal Detachment.” Invest Ophthalmol Vis Sci. 2000;41:3576–3581
- Hammes HP, Du X . “Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.” Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
- Hipkiss AR, Brownson . “Reaction of carnosine with aged proteins: another protective process?” Ann N Y Acad Sci. 2002 Apr;959:285-94.
- Zachary A. Knight, K. Schot Hannan, Matthew L. Greenberg, Jeffrey M. Friedman. “Hyperleptinemia Is Required for the Development of Leptin Resistance.” PLoS ONE 5(6): e11376. doi:10.1371/journal.pone.0011376.
- Min-Diane Li. “Leptin and Beyond: An Odyssey to the Central Control of Body Weight.” The Yale Journal of Biology and Medicine. 2011;84(1):1-7.
- Eri Suganami, Hitoshi Takagi,Hirokazu Ohashi, Kiyoshi Suzuma, Izumi Suzuma, Hideyasu Oh, Daisuke Watanabe, Tomonari Ojimi, Takayoshi Suganami, Yasushi Fujio, Kazuwa Nakao, Yoshihiro Ogawa and Nagahisa Yoshimura. “Leptin Stimulates Ischemia-Induced Retinal Neovascularization: Possible Role of Vascular Endothelial Growth Factor Expressed in Retinal Endothelial Cells.” Diabetes. September, 2004. vol. 53 no. 9 2443-2448
- Joseph R. Vasselli, Philip J. Scarpace, Ruth B. S. Harris, and William A. Banks. “Dietary Components in the Development of Leptin Resistance.” Adv. Nutr. 2013: 4: 164–175.
- Joseph R. Vasselli. “Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance.” Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1365-9. doi: 10.1152/ajpregu.90674.2008. Epub 2008 Sep 10.
- Waltner-Law ME, Wang XL Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem. 2002 Sep 20;277(38):34933-40. Epub 2002 Jul 12.
Jimmy Moore visiting Nally Family Practice . . .
The amazing Jimmy Moore and his wonderful wife, Christine, will be stopping by my office on Monday, September 28th, 2015, between the hours of 9 am and 1pm. Jimmy Moore, Podcaster for Livin’ La Vita Low Carb and author of The Ketogenic Cookbook, KetoClarity and Cholesterol Clarity has been in Phoenix this weekend and agreed to visit the office.
I have been recommending his books and website to my patients for years. His website, books and podcasts have served as superb resources for Low-Carb, High Fat and Paleo dietary programs and patients just starting or fine tuning their programs.
Jimmy and his sweet wife, Christine, have become great friends and trusted colleagues over the years as new science and treatment protocols have been identified in the treatment of obesity, insulin resistance and diabetes. He has been a resource for me and my patients for over 10 years.
Pick up your copy of these books at Barnes & Noble or your favorite nearby bookstore; and if you are in the neighborhood and would like meet Jimmy, bring your copy of the Ketogenic Cookbook, KetoClarity or Cholesterol Clarity to get signed and shake his hand.
If you haven’t checked out his podcasts on Livin’ La Vita Low Carb, or seen his Periscope casts on JimmyScopes.com you need to click on the links and check them out.
The Truth is . . . Caloric Restricted Exercise Won’t Work
This post isn’t going to win me any friends . . . in fact, mentioning this topic a few days ago has already angered a number of them and resulted in an online tongue lashing by a few others. However, I can’t resist. And, based on some very persuasive data and personal experience, I don’t care.
Truth is truth . . . it doesn’t change no matter how you spin it, or attempt to fit it into your paradigm. The problem is what we have accepted in the last 40-50 years as “the scientific truth about getting healthy” is far from truth. By getting healthy, I’m implying the application of main-stream methods accepted to lose weight, reduce cholesterol, improve blood pressure and reduce your risk of heart disease and diabetes.
For the last 40 years we’ve been told that the only way to get and live healthy is to restrict our calories. This main-streamed advise continues even today in our USDA 2010 Dietary Guidelines. And, if you ascribe to this futile dogma propagated since the 1970’s, then you’ll know that the “only acceptable way” to do this is to “eat less fat” (because fat is the most caloric dense of the macro-nutrients, right?) and to “exercise more” (because that’s how we burn calories, right?!) Well, that’s what I thought, too. And that is the health prescription I doled out to my-self and to all of my patients for the first 8 years of my practice.
Interestingly, most of them, including myself, took that prescription of a caloric restricted diet of 1200-1500 calories per day and exercise 3-6 days a week for 30-60 minutes and ran with it. Personally, I restricted calories to 1200-1500 per day and began running triathlons. I performed cardiac monitored running, swimming and cycling for an hour a day during the week and 2 hours on the weekend. I lifted weights 2-3 days per week as well. Guess what it got me? Fat.
It raised my triglycerides by 100 points, elevated my LDL-C and increased my waistline by 3 inches. Yes, I gained weight. But, hey, my doctor was happy because my HDL-C went up by 4 points.
I saw this identical pattern with 3/4ths the patients in my office. A fourth of my patient’s (the group without any genetic insulin resistance) saw weight loss and improvement in their cholesterol profiles, but the rest didn’t. I had the exciting opportunity to introduce the saddened and discouraged 3/4ths of my patients to STATIN drugs and blood pressure medications. My average patient’s gained 2-3% of their body fat each year. Those that exercised like fiends were lucky if their weigh gain just stabilized.
What I saw in my office over a period of eight years was that exercise and caloric restriction didn’t work. But I couldn’t say that, because that goes against everything your 8th grade health teacher taught you. It contradicted your neighborhood dietitian, and it spat in the face of the food pyramid and the USDA Guidelines. The Government wrong? Never. . . . Speaking contradictory of the calorie-in/calorie-out exercise dogma was heresy, right? Contradict, Dr. Ornish, wouldn’t be heard of?!!
If I’ve learned one thing in my medical career, it is this: “Don’t be afraid to question everything” – even Dr. Dean Ornish, the USDA and the American Heart Association. And, fascinatingly, I’m not the only on that did.
——
——
Three Massive Studies did just that . . . question whether this exercise and caloric restriction dogma really works. This is what applying exercise and caloric cutting did for almost 67,000 people between 1972 and 2010 – little to nothing.
WHAT?!! Nothing?! You can’t be serous?
The first of these trials was the MRFIT (Multiple Risk Factor Intervention) Trial. It started in 1972, looking at 12,866 men with high risk for heart disease and followed them over seven years. All of them were placed on caloric restricted low fat diets and encouraged to exercise. It demonstrated that low fat diets and exercise FAILED to reduce weight or stop coronary artery disease in 100% of the cases. Don’t believe me? Read it for yourself (JAMA. 1982; 248 (12):1465-1477).
The second of these trials was the Women’s Health Initiative (WHI). This study started in 1991 and followed 48,835 women (yes, that’s a small city of women) for eight years. They didn’t believe the MRFIT results apparently, so they had a low fat (caloric restricted) arm and a control arm [the SAD diet (Standard American Diet)]. The women on the low fat arm lost a whooping 0.4 kg over the 8 year period (JAMA. 2006 Jan 4;295(1):39-49). 0.4 kg, really!?? That’s almost an entire pound of weight loss over 8 years. Quick, call Barnes & Noble so we can package that diet and sell it on Opra!! (Oh, wait, the news media was a little embarrassed by the findings and never really mentioned them.)
Lastly, if research on 60,000 men and women wasn’t enough to demonstrate what most primary care physicians seen in their offices daily, we had to do the Look AHEAD Study (Action for Health in Diabetes). This study started in 2001 and was supposed to run for 13.5 years. It studied 5,145 Type II diabetic patients with intensive lifestyle intervention. These patients were placed on intensive caloric and fat restriction of 1200-1800 calories per day with exercise and behavioral counseling. It was so unsuccessful, that they stopped the trial at 9.6 years – cause it wasn’t working.
The patients did lose some weight through Look AHEAD . . . an average of 6% of their body fat (That means you would have lost 15.6 lbs over 9 years if you weighed 260 lbs. Successful? . . . NOT). What made this trial worse is that it didn’t improve risk for coronary artery disease and people didn’t live longer (N Engl J Med 2013; 369:145-154). They just got the exciting chance to eat cardboard for 9 years of their lives. Sad. Very sad.
So, what does all this mean? Exercising your brains out at an expensive gym every morning won’t do much more than help you loose 1% of your body fat. It won’t increased your life span and it won’t decrease your risk of heart disease, despite what Dr. Ornish said. If you like spending $40 per month just to stare at sweaty fat bodies jumping up and down in spandex, by all means, please keep going to the gym. But I’d much rather spend that $40 on a nice rib eye steak at a restaurant staring at my wife. But, the benefits of saturated fat . . . that’s for another post.
Don’t get me wrong. I love lifting weights. I love riding my horse. I truly enjoy working in my yard. I even enjoy riding my bicycle. But I do these things now because they bring me peace, decrease my stress, and allow me to connect with nature. Believe me, there’s nothing natural about a 250 pound man in spandex staring at himself in a mirror repetitively lifting 30 pound bars of iron. But, we won’t go there.
My friends, and a few of my patients, get their knickers in a wad trying to decry the fact that I’m giving people a reason not to go running. Maybe I am. To be honest, there’s really only one reason I want to run, . . . and that’s when I’m being chased by a bear. But what good does it do to guilt a person into participation in an activity that isn’t really benefiting their health or help them lose weight, unless they really truly enjoy the activity for the sake of the activity?
Our health is not based upon a caloric scale of inputs and outputs. We are hormonal machines. We gain or lose weight and we gain or lose muscle based on powerful hormone signals, specifically insulin. Simple carbohydrate restriction has profound effects upon our weight, blood pressure, cholesterol and inflammatory states. Until we each come to grips with the fact that the food we eat triggers hormone responses in our bodies, we will continue down the path of diseases of civilization. Hippocrates summed it up when he said, “Let food be thy medicine, and let medicine be thy food.”
Why Your Oatmeal is Killing Your Libido
Have you noticed that there are a large number of advertisements in the media about checking your testosterone or “Low T” Syndrome? It seems like this is the new advertising trend on the radio and late night TV.
Suddenly, everyone’s testosterone is low and men are complaining about their libido, . . . or are they?
If you practice medicine long enough, you’ll see a trend that seems to have arisen as our waistlines have expanded. About half of the men in my office with insulin resistance, pre-diabetes or diabetes have low testosterone levels. But this shouldn’t be a surprise. Type II diabetes, metabolic syndrome and insulin resistance are all driven by an over production in insulin in response to a carbohydrate load in the meal. Patients with these conditions produce between two to ten times the normal insulin in response to a starchy meal. A number of studies both in animal and human models demonstrate that insulin has a direct correlation on testosterone suppression in the blood. This has been demonstrated in both men and women. In fact, glucose intake has been shown to suppress testosterone and LH in healthy men by suppressing the gonadal hormone axis and more predominant testosterone suppression is seen in patient with insulin resistance or metabolic syndrome.
In fact, to put it simply, insulin increases the conversion (aromitization) of testosterone to estrogen in men (it does the opposite in women). Interestingly, Leptin resistance has a similar effect. I tend to see the worst lowering of testosterone in men with both insulin and leptin resistance.
How to you improve your testosterone? Supplemental testosterone has been shown to help, but it comes with some risks, including prostate enlargement and stimulating growth of prostate cancer. The most natural way to improve your testosterone is to change your diet.
A low carbohydrate or ketogenic diet turns down the insulin production and allows the testosterone to be available for use by the body. A ketogenic diet has the effect of reducing leptin resistance as well through weight loss. A simple dietary change of this type is frequently seen in my office to increase testosterone by 100-150 points.
What is a ketogenic diet? It is a diet that restricts carbohydrates to less than 50 grams per day, thereby causing the body to use ketones as the primary fuel source. So, for breakfast tomorrow morning, hold the oatmeal (1/2 cup of Quaker Instant Oatmeal is 31 grams of carbohydrates) and have the bacon and eggs. And, rather than have the cheesecake for desert this evening, have an extra slice of steak butter on your rib-eye and hold the potato.
Sugar with your Salt?
Now you have to watch your salt ingredients too. Store bought salts are starting to add dextrose for flavor. Dextrose is just another word for SUGAR!! Aaarrrrhhhhh!! Why do you need to add sugar to your salt? You don’t. Throw out any salt that contains dextrose. It will raise your cholesterol and cause weight gain.
Never noticed this until it was pointed out by Maria Emmerich. Thanks, Maria.
My Interview with Sam Feltham at SmashTheFat.com
I had the wonderful pleasure of being interviewed by London’s great Sam Feltham from SmashTheFat.com. Thanks for some great conversation Sam!
I look forward to chatting with Sam again soon. Check out the great interviews and coaching that they are offering at SmashTheFat.com
The Obesity Paradox: The Intersection Where Agricultural Policy Contradicts Health Policy
Intent
The intent of this brief is to analyze the burden of obesity in the United States and to recommend policy changes to reduce the medical costs of obesity imposed upon the individual and country as a whole.
Introduction
Conventional fat reduction/caloric restriction guidelines for the treatment of obesity and associated cardiovascular disease, diabetes, cancer, and hypertension have been recommended since the early 1970’s. Because these guidelines are based on questionable evidence, the cost of obesity has dramatically risen to almost 21% of overall health care costs in the United States (1). This brief will analyze the current medical cost of obesity and will explain why the current obesity reduction guidelines perpetuate the problem. In addition, the brief will examine the impact of government agricultural policy on dietary habits, and will recommend changes to farm subsidy legislation in order to reduce the incidence of obesity and decrease costs to the healthcare system.
History & Background
The Cost of Obesity on the Nation
As of 2012, obesity accounts for nearly 21% of overall health care costs in the United States. An obese person incurs $2741 more in medical expenses per year than his or her non-obese counterpart (1). Medicare spending has increased per person per year by $600 for each obese beneficiary (includes out-patient and prescription drugs) and Medicaid beneficiary prescription drug spending increased by $230 per year per obese person. Private insurance has increased by $248 for prescription drugs and $443 for in-patient services for each obese beneficiary per year (2). That adds up to $190.2 billion spent annually on obesity-related medical problems (3). This is a drastic change. Health care costs related to obesity were $85.7 billion (9.1% of overall health care costs) in 2006 and $61.2 billion (6.5% of overall health care costs) in 1998 (4).
The most recent Center for Disease Control statistics reveal that 35.7% of the U.S. adult population is currently obese and another 33% is overweight. Over 78 million adults and 12.5 million children are obese (5). The addition of 30 million people to the health care roles (current estimation of the Affordable Care Act including Medicaid expansion) means that an estimated $27 billion (in 2012 dollars) more will be spent per year on obesity-related health care costs.
Impact of Government Policy on Consumption
The ‘Farm Bill’ was originally enacted as part of President Franklin D. Roosevelt’s Agricultural Adjustment Act of 1933, which provided subsidies to American farmers in the midst of the Great Depression. Since that time the federal government has paid farmers not to grow seven specific crops – known as commodities – with the intent of decreasing the supply, increasing the demand, and thereby raising the price (7). Dr. Susan Blumenthal, former Assistant Surgeon General and current SNAP to Health project director, writes, “The Farm Bill has since expanded to include many different categories or ‘titles.’ The last bill to be authorized, in 2008, had 15 titles, including nutrition (food stamps), crop subsidies, conservation, livestock, crop insurance and disaster assistance. The 2008 Farm Bill approved $300 billion in spending: 67% was spent on food stamps; 15% on agricultural subsidies; 9% on conservation; and 8% on crop insurance” (8).
The U.S. Department of Agriculture (USDA) Subsidy Programs tend to favor, either directly or indirectly, foods that increase obesity and other diseases. These subsidies support commodity crops, specialty crops, dairy products, livestock, and federal purchase programs. Their justification is that they help to stabilize prices in agricultural commodity markets by balancing supply and demand (9). Between 1995 and 2011, $277.3 billion were given in farm subsidies to almost 40% of U.S. farmers. Arizona received $1.1 billion (mainly for cotton); however, only 7% of Arizona farms received subsides during this period (10). These subsidies are incentives to grow and produce specific commodities that have a higher monetary return. Subsidies also act as a disincentive for farmers to grow fruits and vegetables which fall under the “specialty crops” category. This restricts both small and large farmers from diversifying their crops, and limits fruit and vegetable production (11).
Arizona farms received $25.3 million in dairy subsidies from 1995-2011 and $29.5 million in livestock subsidies during that same period (9). Arizona ranks 2nd nationally in its production of cantaloupe & honeydew melons, head & leaf lettuce, spinach, broccoli, cauliflower and lemons, all of which are “specialty crops” and do not receive subsidies (12). The most recent statistics show that the top five states receiving subsidies are Iowa, Texas, Illinois, Nebraska and Minnesota, with Kansas coming in at a close sixth. The majority of these subsidies are for corn ($81.7 billion), soybeans ($26.4 billion), rice ($13.3 billion) and wheat ($34.4 billion) from 1995-2011 (10). It is important to note that the Renewable Fuel Standard of 2012 (legislation protecting the corn-ethanol lobby) mandates that 37% of the corn harvest be used in ethanol production (13).
The food subsidies above have been in place since the Food, Conservation & Energy Act of 2002 and renewed in 2008. They were only to be available for a period of five additional years and were set to expire September 30, 2012. However, the American Taxpayer Relief Act of 2012 (H.R. 8), enacted by Congress and signed into law by President Barack Obama, included provisions that extended these subsidies until September 30, 2013 (20).
For many low-income Americans and especially children, federal programs have a direct and significant influence on food choices. Over 30 million children receive government subsidized school lunch through National School Lunch Program (NSLP) administered by the USDA Food and Nutrition Service (14). USDA-purchased meats, dairy products, grains, fruits, and vegetables are supplied to schools for use in meal programs. Current school lunch recommendations on calorie intake set by the USDA and The Healthy, Hunger-Free Kids Act of 2010mandate school lunches provide 650-850 calories per meal to the 30 million children currently enrolled in this program (15). Interestingly, that is the same caloric count of a Big Mac®, small fry and Diet Coke® from McDonalds® (16). The rational for these purchase decisions are based upon agricultural support goals and adherence to national dietary guidelines (14). A study published in the journal Economics and Human Biology reveals that a person’s body mass index (BMI) increased faster if that personwere on food stamps, and the BMI increased at a faster rate while on the Supplemental Nutrition Assistance Program (SNAP). “We can’t prove that the Food Stamp Program causes weight gain, but this study suggests a strong linkage,” said Jay Zagorsky, co-author of the study and a research scientist at Ohio State University’s Center for Human Resource Research (17). However, much of the food available through the SNAP programs are refined, subsidized high-carbohydrate containing foods.
The price of food influences an individual’s consumption choices (6). Foods that are refined contain increased amounts of sugar or high-fructose corn syrup. These foods contain more caloric density and are often cheaper and more easily accessible. These are foods that are usually found in the center of the grocery store and frequently on sale at the end-caps of each isle. Nutrient-dense, higher fiber foods are frequently associated with higher prices and are consumed less often. These are the foods you usually find around the peripheral areas of the grocery store (fruits, vegetables, etc.) Current food subsidy policy found in the Food, Conservation and Energy Act of 2008 extension mandated by the American Taxpayer Relief Act of 2012 drives up the price of fruits, vegetables, and meats. This policy also turns people toward lower cost foods that are higher in simple carbohydrates and caloric density. Thus, current policy is actually making obesity worse and making America fatter. Research completed at the University of Illinois at Chicago reveals that small taxes or price changes do not produce a change in a person’s BMI; however, more significant price change has a measurable and significant effect on weight in both adults and children. Price increases of 100-150% have been shown to change purchasing behavior and thereby affect health (18). An example of this is the tax levied on cigarette smoking.
The USDA disagrees with the amount of influence they have over the individual American’s food choices. They state openly on their website that “Some public health advocates have argued that falling real, or inflation-adjusted, prices for many high-calorie foods encourage people to buy and consume more of these foods, leading to poor diet quality and rising rates of obesity. A closer look at how consumers respond to food price variation–over time, across geographic markets, in different types of stores, and in response to taxes and subsidies–reveals how food prices affect people’s food choices, and their waistlines. In short, price matters, but not very much, and it is not the only factor” (19).
Why Current Dietary Guidelines Have Not Been Effective
Why do we get fat? Why have we not been successful in losing weight via diet and exercise? The obesity paradox was described by Jules Hirsch of Rockefeller University, who proposed two opposing hypotheses:
- “Obesity is the result of a willful descent into self-gratification” implying that we gain weight because we over-eat (caloric excess) leading to caloric imbalance.
- “Alternative hypothesis is that there is something ‘biologic’ about obesity, some alteration of hormones, enzymes or other biochemical control systems which leads to obesity” (22).
The 1977 Dietary Goals for the United States – the first comprehensive statement by any branch of the federal government about the American diet – supported the first theory. The Guidelines were heavily influenced by the American Heart Association’s position that fat intake alone would cause heart disease. The USDA 2011 Dietary Guidelines imply that the “people who are the most successful at achieving and maintaining a healthy weight do so through continued attention to consuming only enough calories from foods and beverages to meet their needs and by being physically active.” (15)
Current research contradicts the caloric restriction or “calorie in – calorie out” theory. Scientific evidence clearly demonstrates the domino effect of carbohydrate or starch intake increasing insulin levels which thereby stimulates obesity by raising cholesterol and triglyceride levels. Time Magazine recently published evidence that the longstanding recommendations to “eat less high-fat red meat, eggs and dairy and replace them with more calories from fruits, vegetables and especially carbohydrates” is now seen as incorrect (45). Even our medical textbooks from 1965, like the introductory chapter of the Handbook of Physiology, make it clear that carbohydrate intake cause weight gain and raise triglyceride and cholesterol levels (22), (23), (24).
Current Policy
The current version of the Farm Bill was set to expire September 30th, 2013. If it had been allowed to expire, the results would have returned us to the 1949 Farm Bill legislation and theoretically double the price of milk. However, this would have had the effect of freeing up over $5 billion dollars of federal spending per year and would also lead to decreased consumption of a major source of carbohydrates in the standard American diet like wheat and corn. Senator Debbie Stabenow (D-MI), and chairwoman of the Senate Agriculture Committee, had repeatedly said she was opposed to an extension; however, she agreed to a compromise extending the bill for another year to help the farmers experiencing serious drought conditions in 2012 (7). Two additional extensions were passed in the House and Senate, but because these differed so significantly, it was referred to a House-Senate Conference Committee to work out the compromise details. With only $23 billion in spending reductions, The Agricultural Act of 2014 was passed on January 29, 2014 (46).
Outcomes and Stakeholders
If the United States continues its current course, up to 58% of the population will be obese by 2030 (26). Many believe that the USDA Dietary Guidelines are to blame. Richard David Feinman, President of the Nutrition and Metabolism Society and Professor of Cell Biology at SUNY Downstate Medical Center said, “The previous Guidelines have not worked well. It is unreasonable to ask the Dietary Guidelines Advisory Committee (DGAC) to audit its own work. An external panel of scientists with no direct ties to nutritional policy would be able to do a more impartial evaluation of the data. This would be far better for everyone.” (27) A recent Gallup Poll reveals that 63% of Americans believe the USDA Guidelines that a low fat, calorie restricted diet will help in reduction of obesity, and the same study showed that 48% of Americans worry about their weight “all of the time or some of the time” (28). Recent evidence from the Women’s Health Initiative Dietary Modification Trial studying 49,000 women supports Dr. Feinman’s conclusion above. It did not show any statistically significant evidence that following a low-fat or caloric restricted diet had any effect upon obesity (29). Other nutritional experts from the Salt Institute and the National Health Coalition have expressed their support for significant changes to the USDA Dietary Guidelines (30). The Weston A. Price Foundation, which according to its website is “dedicated to restoring nutrient-dense foods to the human diet through education, research and activism,” also supports the view that the current USDA Dietary Guidelines have been a significant cause of obesity and have been an active voice promoting legislative change (31).
On the other hand, the Sugar Association has issued statements that sugar is not the cause of obesity and “continually eating too much food and sedentary lifestyles are the major contributing factors to increasing rates of obesity – not sugar intake” (32). In addition, the American Beverage Association has stated that sugars are not the problem with obesity, but instead, “overweight and obesity are a result of an imbalance between calories consumed and calories burned” (33).
Attempts at modifying the Farm Bill with legislation like the 2012 DeMint Amendment (SA 2276 ) were supported by both Arizona Senators McCain (R-AZ) and Kyl (R-AZ) with a “Yes” vote, as well as Senators Ayotte (R-NH), Brown (R-MA), Burr (R-NC), Coats (R-IN), Coburn (ROK), Cornyn (R-TX), DeMint (R-SC), Graham (R-SC), Hatch (R-UT), Heller (R-NV), Johnson (R-WI), Lee (R-UT), McConnell (R-KY), Murkowski (R-AK), Paul (R-KY), Rubio (R-FL), Sessions (R-AL), and Toomey (R-PA). However, because of a large lobbying agricultural coalition, it was voted down (34). Changing farm subsidies will be a great challenge as 40% of the farmers in the U.S. now have some degree of dependence upon these subsidies. The following agricultural groups have historically had significant monetary interest in the farm subsidies that these amendments would affect:
- American Beekeeping Federation
- American Farm Bureau Federation American Mushroom Institute
- American Sheep Industry Association American Soybean Association
- National Cattlemen’s Beef Association National Corn Growers Association National Cotton Council
- National Council of Farmer Cooperatives National Farmers Union
- National Milk Producers Federation National Pork Producers Council
- National Potato Council
- National Sorghum Producers
- National Watermelon Association
- Produce Marketing Association
- United Dairymen of Arizona
- United Egg Producers
- United Fresh Produce Association
- Western Peanut Growers Association
The following groups have formed coalitions in support of the Farm Bill: Health/Food Justice/Farm Group partnerships, Specialty Crop Farm Bill Alliance, Community Food Security Coalition, Center for a Livable Future at Johns Hopkins University, Collaboration for a Healthy Sustainable Food System, and the Healthy Farms, Healthy People: A Farm & Food Policy Summit for a Strong America.
The American Heart Association’s position is that the Farm Bill needs to be modified to include increased access to fruits and vegetables (35). The American Medical Association’s position in 2008 and 2011 has been for cutting the size and budget of the current Farm Bill (36). The American Osteopathic Association does not currently have a formal position on the Farm Bill.
If certain crops like corn or wheat were no longer subsidized,drastic changes will be likely in the food manufacturing industry, which would likely be the largest proponent against change. Unintended consequences of modifying the Farm Bill and not extending its subsidies could have the short term effect of escalating the price of a number of commodities to two to three times their current price. For example, the price of milk would increase to $6-$8 dollars a gallon without federal subsidies (37). This would likely deter the use of carbohydrates containing dairy products, but may also increase the price of meats and cheeses as well.
The USDA’s Rural Development Progress Report claims that the subsidies it distributed “saved more than 75,000 jobs” in 2006 and over 400,000 jobs in 2011 (38), (39). They claim that without federal farm subsidiesthere would be significant loss of jobs; however, studies from the Cato Institute actually show the opposite.
“Job gains are weak and population growth is actually negative in most of the counties where farm payments are the biggest share of income. Job growth is decidedly weak in the counties most dependent on farm payments. The vast majority of such counties (483) had job gains below the 19 percent national average from 1992 to 2002. A considerable number (167) had outright job losses over the period. In short, farm payments are not yielding robust economic and population gains in the counties where they should have the greatest impact. If anything, the payments appear to be linked with sub-par economic and population growth. To be sure, this quick comparison cannot answer whether growth would have been even weaker in the absence of the payments. Still, farm payments appear to create dependency on even more payments, not new engines of growth” (40).
As of 2010, obesity costs about $73.1 billion per year in lost productivity in the United States (43). The worsening obesity epidemic poses further workforce productivity losses up to 20% more by 2030. Even small improvements in obesity will improve workforce productivity and has substantial potential for savings. Currently, the Affordable Care Act allows employers to charge obese employees 30-50% more for health insurance. Without correcting this epidemic, it may be impossible for many to afford health care, opting out to pay the less expensive tax penalty. This would have the effect of increasing commercial premiums across the country, feasibly pushing private insurance companies out of business and forcing a single payer governmental system.
Recommendations
This brief points out that the overall U.S. healthcare costs associated with obesity have increased by 68% in the last fourteen years. It provides evidence that using current dietary low-fat caloric restriction guidelines show poor statistically significant improvements in obesity. And it provides evidence that obesity is not caused by excessive caloric intake and fat, but by insulin response to carbohydrate intake. Lastly, this analysis provides evidence that the Farm Bill propagates continued worsening obesity rates in the US by providing access to cheap, fattening food.
The USDA 2011 Dietary Guidelines need to be revised to reflect current evidence-based obesity prevention and weight reduction research. The guidelines should include information about limiting the intake of foods high in carbohydrates.
The food subsidy extension provided in the American Taxpayer Relief Act of 2012 was extended five years by the Agricultural Act of 2014. Had it been allowed to expire, it would have saved the country over $200 billion over the next ten years. However, because of so many entitlements involved in this bill, the House and Senate convened in Conference that resulted in a compromise of only $23 billion dollars in spending reductions, the first SNAP reforms since 1996 reducing waste, but did nothing in eliminating subsidies that drive or influence eating behavior (46).
When significant price changes occur, eating behavior will change. As the price of fattening carbohydrates increases, people will eat less of them, leading to a national decrease in obesity and overweight. The current reforms did nothing that will change our dietary behavior.
References
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Insulin Resistance and The Horse
As a family practice physician and bariatrician, my job is to examine and treat the “Diseases of Civilization.” The Diseases of Civilization are those diseases arising out of the changes induced by industrializing and modernizing a society of people. These include diseases like diabetes, dyslipidemia (abnormal cholesterol), heart disease, hypertension, gout, vascular disease, & stroke. It is interesting that the so called Diseases of Civilization didn’t really appear on the scene until the early 1900’s. Yes, we have now identified some of these diseases in the early Egyptians, but to my point, as a society modernizes or industrializes, certain types of disease begin to arise. The Canadian cardiologist William Osler, one of the founding professors of John’s Hopkins Hospital, documented the first “syndrome” associated with narrowing of the arteries causing heart disease at the turn of the 19th century, and in 1912, the American Cardiologist James Herrick is credited with the discovery that narrowed arteries cause angina, a form of chest pain with exertion.
Today we know that underlying each of these diseases is the phenomenon of insulin over production, which seems to arise between five and twenty years prior to the onset of the Diseases of Civilization. Metabolic Syndrome, Dysmetabolic Syndrome or Syndrome X is the name we’ve given to the presentation of three or more of these diseases at once in one person. There is still argument as to whether insulin over production is the chicken or the egg, but what I see clinically has convinced me that insulin is culprit.
Insulin is a very powerful hormone that acts as a key, opening a door in just about every cell in the body, letting glucose (the primary form of fuel derived from carbohydrate) into the cell. For reasons that appear to be genetic, this key becomes “dull” in a portion of the population and does not unlock the door fast enough to lower the blood sugar. So, the body panics, and stimulates production of additional insulin, 2-10 times more in many people. However, the insulin that was produced initially, eventually kicks in. This extra insulin, acting at a slower rate, is the underlying culprit to the Diseases of Civilization.
How, you ask? Let me explain.
Insulin does more than just open the door for glucose.
1. Insulin causes weight gain. It turns on the storage of fat by activating an enzyme called lipoprotein lipase, pulling the triglycerides out of the cholesterol molecules and depositing them in the adipose tissue (fat cells).
2. Insulin raises cholesterol. It drives increased triglyceride production in the liver, especially in the presence of fructose.
3. Insulin triggers atherosclerosis. Triglycerides are essentially the passenger in the LDL (bad cholesterol) molecule. Higher triglycerides cause increased LDL production leading to increased atherosclerosis (narrowing of the arteries).
4. Insulin causes gout & kidney stones. Insulin increases uric acid production and in a round about way can increase calcium oxylate as well, increasing the risk of kidney stones and gout.
5. Insulin raises blood pressure. Insulin stimulates the retention of sodium, causing and increase in blood pressure.
6. Insulin makes inflammation worse. Insulin drives the inflammatory cascade and increases free radicals, and stimulates the inflammatory hormones causes arthritis, allergic rhinitis, psoriasis, dermatitis, and inflammatory bowel problems to be amplified.
My intent is not to demonize insulin. It is an essential hormone, however, when five to ten times the normal amount of insulin is being produced, you’re going to amplify the problems above by five to ten times normal. Type II Diabetes is really just a consequence of 15-20 years of over production of insulin.
This isn’t just something that affects humans. either. We have been seeing this in other species of the animal kingdom as well. Take for example my wife’s horse, Jazz. She’s a beautiful grey Arab/Saddle-Bred who kept having problems with laminitis, or more colloquially known as “founder.” Her diet consisted predominantly of alfalfa at the time, considered a moderate starch containing form of feed.
Laminitis is a progressively increasing tenderness to the hoof of horses or cattle that can be disabling and if not treated appropriately can cause permanent lameness in the animal. Recent literature in the veterinary world have identified that animal diets high in starch have a propensity to cause laminitis as well as colic. First identified in the equine community in the 1980’s with glucose tolerance tests, insulin resistance has been identified as a significant factor in hoof disease. The use of Corn, Oats, Barley or even Alfalfa as a primary form of feed for a horse with insulin resistance greatly increases the risk of laminitis.
Like Jazz, many horses in the arid Arizona climate are fed primarily with oats and alfalfa. Jazz was tested and found to have insulin resistance. Since Jazz has been placed on a much lower starch containing feed, she has had no further problems with laminitis. We converted all our horses to Bermuda grass.
Our family and our horses are all now on Low-Carb diets to some degree and have been for the last seven years. No further hoof problems with the horses, and 55 lbs of weight loss with normalization of cholesterol in their owner, me.
For those with interest, studies reveal feeds in order of the highest to lowest starch (carbohydrate) content to be: Sweet Feed, Corn, Oats, Barley, Wheat Bran, Beat Pulp, Alfalfa, Rice Bran, Soybean hulls, Bermuda Grass. Take a look the Low Carbohydrate help section in the menu above to see the carbohydrate content of many of the foods for human consumption.
It’s time we recognize that our diet and lifestyles have lead us to the Diseases of Civilization, and those diets and lifestyles have even effected our animals.
I Like My Green Eggs & Ham . . .
You know, Dr. Seuss was right, the whole egg is actually good for you.
A recent study from the University of Connecticut demonstrated that eating the whole egg actually decreases LDL (the bad cholesterol) sub-particles and insulin resistance in Metabolic Syndrome better than the egg white or the egg substitute.
I like green eggs and ham!
I do!! I like them, Sam-I-am!
And I would eat them in a boat!
And I would eat them with a goat…
And I will eat them in the rain.
And in the dark. And on a train.
And in a car. And in a tree.
They are so good so good you see!
Fat Thoughts on Cholesterol
As a medical bariatrician and family practitioner specializing in low-carbohydrate diets, I often see the panic stricken look on people’s faces when they look at their cholesterol profiles just after starting a carbohydrate restriction life-style.
First, it is very important to understand that if you check your cholesterol within the first 4-6 weeks of dietary changes, there will be a transient rise in the cholesterol profile as your adipose tissues (fat cells) release your new fuel source into the blood stream and the mitochondria in the one trillion cells in your body convert from the use of glucose to the use of ketones (derived from triglycerides) as the primary fuel source. This is not a problem as the body is designed to handle this increase in triglyceride and cholesterol. I explain to patient’s that we are essentially making the figurative change from “un-leaded fuel to diesel fuel.”
Second, the standard cholesterol profile does not give you a true picture of what is occurring at a cellular level. The standard cholesterol panel checks 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” stands for a calculation usually completed by the lab.
Total cholesterol, HDL and triglycerides are usually measured and LDL-C is measured using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)].
Third, it is also important to realize that HDL and LDL are actually transport molecules (the buses for the triglycerides (the passengers). HDL is taking triglycerides to the fat cells and LDL is taking triglycerides from the fat cells to the muscles and other organs for use as fuel.
When you being a low carbohydrate diet, your blood glucose availability as the primary fuel source drops and triglycerides become the primary source. It takes your body 4-6 weeks to increase the number of mitochondria necessary to effectively use triglycerides as the primary fuel. (This is why many athletes and patients who are active will feel slightly sluggish during their exercise for the first few weeks).
Once your body accommodation to the new fuel, there will be a notable drop in LDL-C and a rise in the HDL.
But this still doesn’t answer the question and relieve the panic seen above. A deep sigh and the look of relief occurs when I explain that LDL-C doesn’t give us the real story.
To make it simple and understandable, LDL is made up of three main sub-types big fluffy ones, medium sized ones, and small dense ones. It’s the small dense ones that contain lipoprotien A [Lp(a)] found in increased vascular risk. Recent studies reveal that heart disease and atherosclerosis is caused by the small dense LDL molecules.
A low carbohydrate diet causes the small dense cholesterol to drop and there is a rise in the two other sub-types This shift in sub-types can actually elevate the Total Cholesterol number and occasionally the LDL-C.
If you are following a low carbohydrate diet, get your cholesterol levels checked. It is more ideal to get an NMR Lipoprofile or VAP Cholesterol test that will give you an LDL particle number and this can be explained more fully by your doctor.
Now, off to the fridge . . . where did I put that package of bacon . . . ?