When I wrote a blog post entitled Lipid Changes on a Very-Low-Carbohydrate Ketogenic Diet about 10 months ago, I knew it would be controversial. Although some people in the low-carb community agreed with my position and conclusions, others thought I shouldn't have revealed my lab results because it would give critics ammunition to use against carb restriction.
I think the jury is still out on the significance of high levels of LDL-C and LDL-P in people following a low-carbohydrate, high-fat diet. My intent is never to offend anyone, and I'm certainly not an expert in this area by any means. But I did want to be 100% honest with people about my own experience and why I wasn't comfortable with those dramatic increases in lipid values. Since writing that post, many ketogenic dieters have contacted me to report similar results and ask how concerned they should be and what they can do to get their numbers moving in the opposite direction. I'm happy to try to help in any way I can, and although I provide information about what has worked for me, I realize that people respond differently to various dietary changes. Also, there are other causes of hyperlipidemia, including major weight loss (1), as well as non-diet-related reasons, such as hypothyroidism.
My follow-up NMR last June revealed improvement two months after making changes to my diet, but I didn't know if my numbers would continue to decline, stabilize, or increase over time. I've been eating a high-fiber, low-carb. lower-saturated-fat diet for about a year, and I recently decided to have another NMR (Nuclear Magnetic Resonance) spectroscopy LipoProfile done to see how things were progressing.
April 2015 NMR results
I'm really pleased with these results. My total LDL-P has dropped by 250 mmol/L and is now borderline-high, as is my LDL-C, which has further declined from 177 mg/dL last June. My small LDL-P has always been low, but it's now less than 90 mmol/L.
Elevated LDL-C, LDL-P, Insulin, and Cardiovascular Disease Risk
How important are LDL-C and LDL-P in terms of cardiovascular disease (CVD) risk? It depends who you talk to. I respect the opinions and expertise of the professionals below and believe they all provide valid arguments.
I asked Dr. Thomas Dayspring to review my most recent NMR report. He feels that although my LDL-P has improved, it still places me at greater than average risk for a cardiac event. He said that given my age and the fact that I'm in the latter stages of perimenopause, I should definitely monitor this and other values and make appropriate lifestyle adjustments as needed. Also, there's no arguing that I carry a lot of cholesterol in my HDL particles as well as LDL particles, and this cholesterol is transferred back and forth between all the particles within the bloodstream. He questioned whether the excess cholesterol is due to hyperabsorption, hypersynthesis, increased lipoprotein production and lipidation, or decreased clearance. Without further testing, there's no way to know for certain.
Dr. Dayspring is a very progressive lipidologist, and I highly recommend his LecturePad presentations (sign up for free, and you'll be able to access all content). In Part 1 of Have Cholesterol Measures Outlived Their Usefulness, he explains the reason oatmeal and other whole grain cereals aren't a good choice to increase fiber intake for most people, why triglyceride levels should optimally be less than 100 mg/dL, and the dangers of relying on LDL-cholesterol measurements to evaluate degree of cardiovascular risk. In Part 2, he discusses the importance of controlling insulin resistance (IR); the interplay between hyperinsulinemia, hyperleptinemia, and appetite; and the benefits of carbohydrate restriction for those with metabolic syndrome: "Dr. Atkins was right."
Although in my other blog post I referred to an article where he recommended statin therapy for anyone with an LDL-C level greater than 190 mg/dL, more recently, he said:
"That was written some time ago. I'd now amend that everyone with moderate to high lifetime risk for CVD events as determined by lipid/lipoproteins, family history, examination (BP, xanthomata) and smoking history - not simply LDL-C by itself."
Dr. Dayspring also provides interesting information in the Cellular Regulation of Sterols lecture series, including the fact that vegans (who consume no animal products and therefore no cholesterol) absorb the same amount of cholesterol from the gut as do meat eaters and lacto-ovo vegetarians (about 55%, on average), but in their case, it's entirely biliary in nature as a result of the gallbladder releasing hepatic cholesterol into the intestine. Even in non-vegans, most of the cholesterol in the gut comes from the bile rather than the food we eat, which is why limiting egg consumption doesn't make sense as a strategy for lowering cholesterol levels. Even people who absorb more cholesterol than average ("hyper-responders") experience only mild elevations in serum cholesterol concentrations when dietary cholesterol is increased (2).
Ivor Cummins is a chemical engineer known on social media sites as The Fat Emperor and is a prolific blogger on his website of the same name. He's spent a great deal of time studying and writing about the role insulin and a high-carbohydrate diet play in CVD risk. While he agrees with Dr. Dayspring that LDL-P count is important, he feels that the combination of small, dense LDL particles and high insulin levels are the root cause of coronary artery disease (CAD) (3). He also believes maintaining adequate vitamin D3 levels is crucial to cardiovascular health, and I've recently seen him advise people with genetic defects (such as ApoE4) and very elevated LDL-P to replace a portion of saturated fat with monounsaturated fat and long-chain omega-3 fats. In addition to blog posts, he has several great videotaped lectures on his website, including "The Cholesterol Cunundrum."
Dr. Peter Attia is a very-low-carbohydrate, ketogenic diet proponent who believes that elevated LDL-P values warrant dietary modification, including reduction in saturated fatty acid (SFA) intake. In a recent blog post, he describes a patient whose LDL-P dropped from 3500 to 1300 as a result of cutting saturated fat intake down to 25 grams per day while remaining on a ketogenic diet. He goes on to say:
"While I believe the population-based guidelines for SFA are not supported by a standard of science I consider acceptable, it does not imply I believe SFA is uniformly safe at all levels for all individuals."
A few years back he wrote a 9-part series of blog posts entitled The Straight Dope on Cholesterol, which received a lot of attention and great feedback. Unfortunately, I've only read the first 2 parts at this point, but I'm hoping to read the entire series soon.
Dr. Spencer Nadolskey is a family physician who promotes a whole foods diet and healthy lifestyle. He's recently done some experimenting with different diets (low-carb and vegan) and reported the changes in his biomarkers with each. He has a very balanced and moderate approach to health and wellness, recognizing the importance of taking people's preferences and individual responses into account when making dietary recommendations.
As I said in my original blog post, most people who follow a low-carbohydrate, high-fat diet don't experience significant elevations in lipids as I did, although it's estimated that at least 25% do. In fact, Dr. Attia states in the blog post I linked to above that even when he was consuming 40% of his calories as saturated fat while following a very-high-calorie ketogenic diet, his biomarkers actually improved.
Increased vs. Decreased Risk for Cardiovascular Disease
ApoE genotype Apolipoprotein (Apo) E is a regulator of plasma lipid levels. I have two copies of the ApoE3 gene (3,3), which carries a low risk for atherosclerosis and cognitive disorders including Alzheimer's disease (4). Those with the ApoE4 genoptye, who often have elevated cholesterol levels and are at increased risk for developing CAD, dementia, and other diseases, may find the ApoE4 Forums Heart Disease Discussion helpful for information and support.
Family history Regardless of genetic markers, a strong family history of heart disease is another risk factor for a cardiac event. Allthough I don't have the ApoE4 genotype or familial hypercholesterolemia (FH), several of my family members have had CAD. My mom, who has stable atherosclerosis, has been on a low-dose statin for over 10 years. She is thin, active, and has never had any markers of insulin resistance (her lipid profile is remarkably similar to my own), although she was a long-term smoker before quitting eight years ago.
BMI and waist-to-hip ratio (WHR) My BMI is 19 (under 23 is optimal), and my WHR is 0.7 (less than 0.8 is optimal for women in terms of cardiac risk).
LDL-P Larger particles are generally considered less atherogenic than small, dense particles. I have very low small LDL-P and borderline-high LDL-P. While some would argue that my large LDL-P poses no concern, it's still higher than what's considered optimal. Also, in a study published after my initial blog post, large numbers of small and large LDL particles were both associated with increased CVD risk when compared with medium LDL particles (5). In addition, the MESA study researchers, who investigated CAD risk in more than 5000 people, reported this finding regarding carotid intima thickness (CIMT or IMT), a measure of subclinical atherosclerosis in the walls of the artery:
"Without accounting for LDL subclass correlation, small LDL and smaller LDL size were associated with IMT but large LDL was not. However, after accounting for their inverse correlation, both LDL subclasses showed highly significant and independent associations with IMT, with a greater difference in IMT per large LDL particle compared with small LDL. Smaller LDL size was no longer significant after taking into account the particle concentrations of the two LDL subclasses and risk factors. Thus, small LDL was a strong confounder of the association of large LDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic (6)."
Triglycerides, HDL-C, and HDL-P Low fasting triglycerides, high HDL cholesterol, and a large number of HDL particles are considered cardioprotective. Fortunately, I meet the criteria for all three. However, per Dr.Dayspring, my HDL-C/HDL-P ratio of 67 suggests potential dysfunction:
"In a recent study, individuals with the highest HDL-C/HDL-P ratios (>53) had a significant 1.5-fold increase risk for atherosclerosis progression compared with individuals with the lowest HDL-C/HDL-P ratio (<41) (7)."
However, at this point we don't really know whether my risk is increased, and I'm comfortable with these values but will continue to monitor them.
Interestingly, 4 years ago, when I was following a low-fat diet with at least 50% of calories from carbohydrate, my triglycerides were 55 mg/dL, and my HDL was already quite high at 79 mg/dL. I think it's safe to say that I'm not inherently insulin resistant.
Insulin levels I've had fasting insulin tested three times within the past three years, and each time my level was between 1 and 2 mIU/mL, which is considered very low ("Normal" ranges from 1 to 10 mIU/mL). Researchers have known about the connection between elevated insulin levels and heart disease risk for decades (8), and Ivor Cummins has discussed this extensively on his blog and in his lectures.
Fasting blood glucose, postprandial blood glucose, and A1c Elevated blood glucose, even at prediabetes levels, causes damage to endothelial cells that greatly increases CVD risk (9). My fasting blood glucose levels are consistently in the 80s, and 1-2 hours after eating, I am always under 130 mg/dL. I have an A1c every 6 months, and it has been 5.1-5.2% for the past 3 years. Prior to going low carb, my A1c was 5.6%, and my postprandial blood glucose values were routinely higher than 160 mg/dL.
Age I'll be 49 this year, and as stated above, I'm transitioning into menopause, when changes in hormones, lipids, and body fat distribution increase CVD risk (10).
Low-carbohydrate diets are clearly beneficial for reducing CVD risk in people with metabolic syndrome and type 2 diabetes (11). But what about people with type 1 diabetes or those like me, who don't have IR but follow a carbohydrate-restricted lifestyle for blood glucose issues, weight control, or simply because they feel better when they eat this way?
I track what I eat in My Fitness Pal most days and have been doing this for over a year. While the nutritional information for the food database isn't completely accurate (as I'm sure anyone who uses it would agree), it does give a good general idea of caloric and macronutrient intake.
Carbohydrates: I eat 30-45 grams of net carbohydrate per day consistently. Carb sources include nonstarchy vegetables, berries, Greek yogurt, cottage cheese, nuts, and dark chocolate.
Fiber: My fiber intake is very high, roughly equal to my net carb intake. A typical day includes half a large avocado, 1 cup of blackberries or raspberries, 2-3 oz unsweetened chocolate or cocoa (more than half the carbs come from fiber), 2 Tbsp flaxseed and/or chia seeds, 3-4 oz nuts, and 4-6 cups of nonstarchy vegetables. Fiber helps lower cholesterol levels yet doesn't appear to compromise absorption of fat-soluble vitamins and other nutrients (12).
Total Fat: According to My Fitness Pal data, my fat intake ranges from 80-100 grams, which is around 50-60% of my caloric intake (I'm usually between 80-90 grams). Monounsaturated fat accounts for the largest percentage, and primary sources are avocado, olives, nuts, and meat. Eating fatty fish like sardines or salmon 3-4 times a week ensures that I get plenty of long-chain omega-3 polyunsaturated fats, including docosahexaenoic acid (DHA), which is anti-inflammatory and believed to be cardioprotective (13).
Saturated Fat: I don't deliberately set a limit, but I generally end up consuming 20-30 grams of saturated fat daily. Although I'm usually on the lower end of that range, this still allows for modest amounts of cheese, half-and-half, coconut oil, butter, and fatty meat.
Protein: I've discovered that I feel best and most energetic with a relatively high protein intake of around 100 grams per day, which is just over 1.75 grams per kilogram body weight.
Am I in ketosis? I rarely check urine ketones anymore, but when I do they're usually trace or negative. Ketosis has never been my goal (aside from the 3-month experiment I discussed in the prior blog post); keeping blood glucose levels and other biomarkers under control, looking and feeling my best, and eating a healthy, well-balanced diet are what's important to me. However, I realize that for some people, ketosis can be beneficial and desirable.
What about having Coronary Artery Calcium (CAC) scoring, a CIMT, or other tests to rule out subclinical atherosclerosis? According to Dr. Dayspring, CAC testing isn't advisable for women younger than 60, who usually get a zero score even if trouble is brewing. He believes that a CIMT can be useful if done correctly.
Here are his recommendations for further testing in my case, some of which I've already had done. I plan to do the rest within the next year or so.
Sterol synthesis and absorption markers
Omega 3 index
Inflammation markers: MPO, Lp-PLA2, hs-CRP
Once per lifetime tests: ApoE, MTHFR genotypes and Lp(a) level (I'm negative for ApoE and MTHFR genotypes but haven't had Lp(a) done yet)
Homocysteine (I received a score of 8 on a scale of 4-15 umol/L when last done 2 years ago)
Vitamin D (50 ng/ml as of February 2015, which is considered within the optimal range)
On Not Taking Sides
I'm a very moderate person. I don't like confrontation and dislike the "us vs. them" mentality. It probably won't come as any surprise that I'm a registered independent and vote Democratic as often as I do Republican (and increasingly frequently for another party altogether). In addition to the experts listed above, I like and respect the diversity of opinions on this subject that have been voiced by many other knowledgeable people, whether or not they're advocates of carbohydrate restriction.
It's generally agreed within the low-carb community that people have different levels of carbohydrate tolerance. So why is it considered heresy to propose that the same might be true with respect to optimal saturated fat intake?
As I said earlier, I think we still don't know enough about what kind of risk elevated LDL-P and very high LDL-C carry in the setting of a very-low-carb diet where other markers improve. Because of this, I choose to eat in a way that allows me to enjoy all the benefits of carbohydrate restriction yet keeps my LDL particle number at a level I feel comfortable with. Some may think I've gone too far in making changes to my diet in order to improve my numbers; on the other hand, I'm sure there will be others who feel I haven't gone far enough, since my levels still aren't considered "optimal." I understand both points, but I have to go with my gut on this one. Ultimately, it's up to you to decide what feels right for you given what we currently know and don't know.
1. Phinney SD, et al. The transient hypercholesterolemia of major weight loss. Am J Clin Nutr. 1991 Jun;53(6):1404-10.
2. Fernandez ML. Effects of eggs on plasma lipoproteins in healthy populations. Food Funct 2010 Nov;1(2):156-60
3. Phillips MC. Apolipoprotein E isoforms and lipoprotein metabolism. IUBMB Life. 2014 Sep;66(9):616-23
4. Lamarche B, et al. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. JAMA. 1998 Jun 24;279(24):1955-61.
5. Grammer TB, et al. Low-density lipoprotein particle diameter and mortality: the Ludwigshafen Risk and Cardiovascular Health Study. Eur Heart J. 2015 Jan 1;36(1):31-8.
6. Mora S, et al. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2007 May;192(1):211-7.
7. Qi Y, et al. Cholesterol-overloaded HDL particles are independently associated with progression of carotid atherosclerosis in a cardiovascular disease-free population: a community-based cohort study. J Am Coll Cardiol. 2015 Feb 3;65(4):355-63.
8. Després JP, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med. 1996 Apr 11;334(15);952-7.
9.Maschirow L, et al. Inflammation, coagulation, endothelial dysfunction and oxidative stress in prediabetes - Biomarkers as a possible tool for early disease detection for rural screening.2015 Mar 6. pii: S0009-9120(15)00071-5.
10. El Khoudary SR, et al. Progression Rates of Carotid Intima-media Thickness and Adventitial Diameter during the Menopausal Transition. Menopause (New York, NY). 2013;20(1):8-14.
11. Volek JS, Feinman RD.Carbohydrate restriction improves features of the Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab(Lond) 2005 ;2:31.
12. Ramprasath VR, et al. Consumption of a dietary portfolio of cholesterol lowering foods improves blood lipids without affecting concentrations of fat soluble compounds. Nutrition Journal. 2014;13:101.
13. Richard D, et al. Infusion of docosahexaenoic acid protects against myocardial infarction.ProstaglandinsLeukot Essent Fatty Acids.2014 Apr;90(4):139-43.
As a registered dietitian and certified diabetes educator, I'm required to complete 75 hours of continuing education (CE) every five years. Fortunately, there are many ways to fulfill this requirement, including watching webinars, attending conferences, and completing exams on nutrition-related books. Although my recertification date is more than a year away, I've been trying to complete as many CE units as I can ahead of time, including a short course on nutritional management of Polycystic Ovary Syndrome (PCOS).
Although the author of the course gave a good overview of the disease and recommended avoiding refined carbohydrates, I found that several of the dietary suggestions were not particularly helpful for many women who struggle with PCOS, such as:
PCOS is one of the most common endocrine disorders among reproductive-aged women, as well as the leading cause of infertility. Instead of an egg being released from one of the follicles in the ovaries on a monthly basis as occurs in normal ovulation, a hormonal imbalance (too much luteinizing hormone and not enough follicle stimulating hormone) results in the egg failing to mature; instead, the follicle forms a small cyst. This process is repeated, and eventually the ovaries contain dozens of these cysts. Although the clinical presentation varies from person to person and some women have few symptoms, its hallmarks are insulin resistance and hyperinsulinemia. Other common features include:
Women with PCOS are more than twice as likely to meet the criteria for metabolic syndrome as those without the disorder; in fact, in one study, women between the ages of 20-39 were found to have a 4-fold to 8-fold increased prevalence of metabolic syndrome compared to women of the same ages in the general population (1). Those with both PCOS and metabolic syndrome are therefore at much higher risk for developing type 2 diabetes and cardiovascular disease. Since research has demonstrated that carbohydrate restriction improves markers of insulin resistance (IR) and other features of metabolic syndrome (2), it would seem logical to consider it an appropriate -- if not the most appropriate -- diet for PCOS. Even nonobese women with PCOS experience IR, though, and are at increased risk for progression to diabetes in the future.
A small 2005 study evaluating the effects of a ketogenic diet on women with PCOS found significant improvements in fasting insulin, body weight, and hormone levels among subjects who completed the study -- including two pregnancies in women who had previously been unable to conceive (2).
This is why I find it disappointing to read recommendations like those given in the PCOS course, which sound very similar to the one dietitians often make for people with diabetes. While this type of diet may work for insulin-sensitive people, it simply doesn't result in beneficial outcomes for most women with insulin resistance and hyperinsulinemia. For people with defective hormonal regulation, it can be difficult to control insulin levels and appetite when eating more than minimal amounts of carbohydrate.
The authors of a recent review looking at six different diets and their effects on physiological and psychological outcomes in women with PCOS came to the following conclusion: "Weight loss should be targeted in all overweight women with PCOS through reducing caloric intake in the setting of adequate nutritional intake and healthy food choices irrespective of diet composition (4)."
While the researchers noted moderate to severe bias among all the studies, I found some other issues:
The other three studies didn't look at "low-carb" diets per se but found less depression and lower triglycerides in subjects consuming higher amounts of protein and improvements in insulin sensitivity among women following a low GI diet.
My point is that aside from one small study, researchers haven't attempted to investigate whether a very-low-carbohydrate diet containing adequate calories is effective in improving IR and hyperinsulinemia, promoting weight loss, and improving hormonal balance in order to reduce masculinization and facilitate ovulation. However, I've read anecdotal reports where carb restriction did improve symptoms, and at least one woman I've worked with definitely experienced benefits. There's also the spontaneous decrease in caloric intake that occurs for many, although not all, people who consume a carbohydrate-restricted diet (8).
Now, I'm not claiming that low-carb diets work for everyone or that they're the only thing needed to achieve results. Certainly insulin-sensitizing medications such as metformin, stress management, exercise, support groups, and supplements play a large role in managing PCOS as well. But for the overweight woman suffering from this disorder, I don't feel that it's enough to simply encourage weight loss without providing guidance on how to do so in a sustainable way that has been shown to improve IR and insulinemia -- i.e., limiting carbs to 50 net grams per day or less.
I understand that some women with PCOS may not want to follow a carb-restricted diet, and I certainly respect and support everyone's right to make dietary choices. But I believe dietitians and other healthcare professionals who work with women who struggle with PCOS should present a low-carb diet as an option rather than insist that everyone consume "a minimum of 130 grams of carbohydrate per day." Unless you have lived with PCOS, diabetes, or metabolic syndrome and tried carbohydrate restriction, it's impossible to understand what an impact making this type of change could have on your health and quality of life.
* Please speak with your doctor or health care provider prior to making any changes to your diet.
1. Apridonidze T, et al. Prevalence and Characteristics of the Metabolic Syndrome in Women with Polycystic Ovary Syndrome. J Clin Endocrinol Metab. 2005 Apr;90(4):1929-35
2. Volek JS, Feinman RD.Carbohydrate restriction improves features of the Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab(Lond) 2005 ;2:31
3. Mavropoulos JC, et al. The effects of a low-carbohydrate, ketogenic diet on the polycystic ovary syndrome: A pilot study. Nutrition & Metabolism. 2005;2:35
4. Moran IJ, et al. Dietary composition in the treatment of polycystic ovary syndrome: a systematic review to inform evidence-based guidelines. J Acad Nutr Diet. 2013 Apr;113(4):520-45
5. Douglas CC, et al. Role of diet in the treatment of polycystic ovary syndrome. Fertil Steril.2006; 85(3):679-688
6. Stamets K, et al. A randomized trial of the effects of two types of short-term hypocaloric diets on weight loss in women with polycystic ovary syndrome. Fertil Steril. 2004;81(3):630-637
7. Moran LJ, et al. Short-term meal replacements followed by dietary macronutrient restriction enhance weight loss in polycystic ovary syndrome. Am J Clin Nutr. 2006;84(1):77-87
8. Westman EC, et al. Low carbohydrate nutrition and metabolism. Am J Clin Nutr.August 2007; 86(2):276-284
Over the past few months, several women have contacted me expressing frustration at being unable to lose weight despite strictly following a LCHF diet. When I ask whether they're including high-fiber plants like brussels sprouts, berries, nuts, and dark chocolate, the response is typically, "I avoid those because they're so high in carbs. I limit my carbs to less than 20 grams total." This is the trend I've noticed lately in the low-carb community: the belief that limiting vegetables and other high-fiber plants in an attempt to keep carbohydrate intake at an absolute minimum (sometimes as low as 10 grams of total carbohydrates per day) long term is the key to losing weight.
Soluble Fiber's Role in Improving Blood Glucose Regulation
A few weeks ago, Martina from the KetoDiet App website wrote an excellent blog post about counting net carbs vs. total carbs for those following a carbohydrate-restricted lifestyle. In the article, she correctly states that insoluble fiber passes through your system without being absorbed, so it should be subtracted from the total carbohydrate count. In addition, Martina explains that, unlike insoluble fiber, soluble fiber does not pass through the colon but rather is fermented into short-chain fatty acids (SCFAs) by our gut bacteria.
The principal SCFAs are acetate, butyrate, and propionate. Of these, propionate is the only one that can be converted into glucose via gluconeogenesis (1). But would this have any significant effect on postmeal blood glucose given that most fiber is insoluble and only 15-40% of any soluble fiber will be converted to propionate (2)? Take brussels sprouts, for instance, one of the few foods that contains more soluble than insoluble fiber. A 1-cup serving has about 4 grams of soluble fiber. Less than 2 grams will be converted into propionate, and the amount of glucose produced from it via hepatic gluconeogenesis would be quite small, so serum blood glucose levels wouldn't be affected much.
More importantly, as Martina pointed out, De Vadder, et al, recently reported the results of a study on mice suggesting that SCFAs promote intestinal gluconeogenesis (IGN), with propionate acting as substrate and butyrate promoting the expression of genes necessary to induce this process. Compared with control mice fed their normal diet, mice who were fed diets enriched with SCFAs and fructo-oligosaccharides (FOS) experienced lower fasting serum blood glucose levels, improved glucose tolerance, and a significant reduction in the enzyme responsible for hepatic gluconeogenesis (3). Essentially, propionate is converted to glucose, which is used within the intestine, decreasing the amount of glucose produced by the liver, resulting in the above-mentioned benefits. Yes, this was an animal study, but it provides an intriguing explanation for the improvement in blood glucose levels seen in human studies examining the role of dietary fiber (4, 5).
Blood glucose response to fiber-rich food may differ among some people with Type 1 diabetes, whose blood glucose levels can reportedly rise as a result of higher food volume in the stomach or other stimuli, regardless of digestible carbohydrate intake. Dr. Bernstein and others with T1 have suggested such a response (what he calls The Chinese restaurant effect), but I know of no studies confirming this and would appreciate references if anyone has them.
Health Benefits of Fiber and SCFAs
We've known about the benefits of fiber on colon health for decades. Although it's believed these are due in part to insoluble fiber's ability to reduce intestinal transit time so potentially carcinogenic substances in our food spend as little time as possible in our GI tract, more recent research suggests that fiber's chemoprotective effects may be due primarily to the effects of one of the SCFAs, butyrate (6,7), which provides energy and nourishment for the cells of the colon.
In addition, higher fiber intakes may reduce levels of C-reactive protein (CRP) and other inflammatory markers, improve our immune response, and protect the gut from harmful microorganisms that can make us ill (8). In essence, fiber's fermentation to SCFAs helps keep our gut well nourished and working the way it should.
Increasing High-Fiber Carbohydrate Intake May Be Helpful for Weight Loss
Let's go back to restricting intake to less than 20 grams of total carbohydrates in order to lose weight. When carbohydrate intake is this low, there's a limited number of foods that can be eaten: meat, cheese, fish, eggs, butter, cream, coconut oil, olive oil, and small amounts of greens and other very-low-carb vegetables. Yes, carbohydrate intake may be well below 20 grams of total carbs daily, but depending on portions consumed, calorie/energy intake may be too high to promote weight loss. A serving of bullet-proof coffee contains 440 calories, zero carbs, zero protein, and zero fiber.
Aside from fiber's beneficial effects on overall health outlined above, consuming at least a moderate amount of fiber can facilitate weight loss, and both insoluble and soluble fiber can be helpful in this regard.
Insoluble fiber passes through the body without being absorbed. It adds volume to meals, but zero calories and zero carbohydrates. In fact, you could almost say that insoluble fiber provides negative calories, in that it may lower the amount of energy derived from fat and protein when all three are consumed at a meal (9). Most foods are higher in insoluble than soluble fiber, with a few exceptions (Please refer to Martina's fiber chart in the blog post linked to above).
Soluble fiber does contribute calories/energy to the body, but no carbohydrates. The chief benefits provided by soluble fiber are due to its fermentation to the SCFAs acetate, butyrate, and propionate, which have been shown to promote satiety, reduce intake, and and decrease body fat (3,10-11).
Carbohydrate and Fiber: What's Optimal?
Like carbohydrates, fiber is another substance where across-the-board recommendations can't be made, but I think it's best to aim for at least 20 grams daily, with 1/3 or more from soluble fiber. If you're limiting yourself to less than 20 grams of total carbohydrate, the maximum amount of fiber you can possibly get is 18 grams, and that's only if the carbs come from foods that are more than 90% fiber, such as chia seeds, flaxseed, or avocado. Generally speaking, those who consume diets containing less than 20 grams of total carbohydrate end up with 10 or fewer grams of fiber. Some people reportedly consume less than 5 grams on a consistent basis.
The goal of carbohydrate restriction is to keep blood glucose and insulin levels low, and this can be accomplished without reducing carbs to near-zero levels. I consume around 30-45 grams of fiber daily, and my net carb intake is around 35-50 grams, so my fiber to nonfiber carb ratio is roughly 1:1. This works well for me, but some people do better with 20-30 grams of fiber and slightly lower net carb intake. People with certain GI disorders* may require restriction of certain types and amount of fiber.
How do you get to 30 grams of fiber yet still maintain net carb intake of less than 40 grams? Here's one of the sample menus with recipes that will be included in my upcoming book, The Low Carb Dietitian's Guide to Health and Beauty.
Sample Low-Carb, High-Fiber Menu
Cinnamon Flaxseed Pudding*
1 cup blackberries
Coffee or tea with 2 Tbsp half and half
1/2 oz dark chocolate (at least 85% cocoa)
Water, tea, or other sugar-free beverage
3 celery stalks with 1 Tbsp almond butter
Chocolate Avocado Pudding*
Water, tea, or other sugar-free beverage
Protein: 88 grams
Total Carbohydrates: 68 grams
Fiber: 31 grams
Insoluble Fiber: 20 grams
Soluble Fiber: 11 grams
Net Carbohydrates: 37 grams
Fat: 108 grams
Cinnamon Flaxseed Pudding
Number of Servings: 1
½ cup cottage cheese
2 Tbsp ground flaxseed
½ tsp cinnamon
3 Tbsp chopped toasted pecans
Stevia or other sweetener, if desired
Combine all ingredients in small bowl.
Number of Servings: 1
4 oz fresh mozzarella cheese, sliced into ¼-inch rounds
1 large vine-ripened tomatoes, sliced ¼-inch thick
1/2 cup fresh basil leaves
Coarse sea salt, to taste
2 Tbsp cup extra-virgin olive oil
On a plate, alternate mozzarella slice, then tomato slice, followed by basil leaf, and repeat sequence, overlapping each item slightly. Sprinkle salt and drizzle olive oil over top.
Number of Servings: 4
2 Tbsp coconut oil
1 cup chopped onion
2 tsp sea salt
2 tsp chopped garlic
2 tsp ground ginger
2 tsp coriander
1 tsp turmeric
1 tsp chili powder
4 cups broccoli florets
2 cups snow peas
2 cups mushrooms
½ cup coconut milk
1 lb chicken breast, cut into bite-sized pieces
Heat oil in a wok or large saucepan over medium-high heat. Add the onion, then cook and stir until browned. Mix in garlic and spices. Add broccoli, pea pods, and mushrooms. Cook and stir for 1-2 minutes.
Add coconut milk and chicken. Reduce heat to medium and cook for 7 to 8 minutes, until chicken is no longer pink. Stir and remove from heat. Serve immediately.
Chocolate Avocado Pudding
Number of servings: 4
2 medium very ripe avocados
½ cup unsweetened coconut milk
½ cup unsweetened cocoa powder
1 cup erythritol or other granulated sugar substitute equivalent to sweetness of ¾ cup sugar
2 tsp vanilla extract
Cut avocado in half, remove pit, and scrape flesh into food processor or blender. Add coconut milk, cocoa powder, sweetener, and vanilla extract. Process until ingredients are well combined and there are no lumps of avocado. Divide into four dishes and refrigerate at least 30 minutes or until ready to serve.
Roasted Brussels Sprouts Recipe
And for anyone who was hoping for a brussels sprouts recipe after seeing the photo and reading about their high soluble fiber content, please check out this delicious side dish, Roasted Brussels Sprouts with Pecans, from Kalyn's Kitchen.
A Balanced Low Carb Diet: Eat Plenty of Plants and Animals
If you're consuming less than 20 grams of carbohydrate daily and achieving your weight loss goals, I'm very happy for you. But I would consider adding at least a few grams of high-fiber carbohydrates -- such as vegetables, berries nuts, and dark chocolate -- to optimize overall health and increase your likelihood of long-term success. And if your weight loss has stalled, I definitely recommend increasing your intake of these foods and perhaps decreasing fat and increasing protein intake, depending what you're doing currently. A sustainable low-carb lifestyle consists of a balance of nutritious animal and plant foods, based on personal tolerance, preferences, and goals.
* * *
*For those with small-intestinal bacterial overgrowth (SIBO) or other conditions requiring a low-reside diet, such as acute diverticulitis or other inflammatory bowl conditions, the recommendations for fiber intake provided in this article may be contraindicated. Consult your healthcare provider, who can provide guidance or refer you to a dietitian for recommendations.
1.Mithieux G, et al. Intestinal glucose metabolism revisited. Diabetes Res Clin Pract. 2014 Sep;105(3):295-301
2. Bergman EN, et al. Energy contributions of volatile fatty acids from the gastrointestinal tract in various species. Physiol Rev. 1990 Apr;70(2):567-90
3. De Vadder F, et al. Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits. Cell. 2014 Jan 16;156(1-2):84-96
4. Post, RE, et al. Dietary Fiber for the Treatment of Type 2 Diabetes Mellitus. J Am Board Fam Med Jan-Feb; 25:16-23, 2012
5. Aller R, et al. Effect of soluble fiber on lipid and glucose intake in healthy subjects: a randomized clinical trial. Diabetes Res Clin Pract. 2004; 65(1): 7-11
6. Cho Y, et al. Colon cancer cell apoptosis is induced by combined exposure to the n-3 fatty acid docosahexaenoic acid and butyrate through promoter methylation. Exp Biol Med (Maywood) 2014;239(3):302-310
7. Fung KY, et al. A review of the potential mechanisms for the lowering of colorectal oncogenesis by butyrate. Br J Nutr. 2012 Sep; 108(5):820-31
8. Levison ME, et al. Effect of Colon Flora and Short-Chain Fatty Acids on Growth In Vitro of Pseudomonas aeruginosa and Enterobacteriaceae. Infect Immun. Jul 1973; 8(1): 30–35
9. Baer DJ et al. Dietary fiber decreases the metabolizable energy content and nutrient digestibility of mixed diets fed to humans. J Nutr. 1997 Apr;127(4):579-86
10.Darzi J, et al. Do SCFA have a role in appetite regulation? Proc Nutr Soc. 2011 Feb;70(1):119-28
11. Lin HV, et al. Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. PLoS One. 2012;7(4):e35240
Last month, Diabetes Care, a journal of the American Diabetes Association, published an article linking sulfonylurea use to increased risk of cardiovascular disease in women. Sulfonylureas stimulate the pancreas to produce insulin and include glipizide (Glucotrol), glyburide (Micronase), and glimepiride (Amaryl) in the US, as well as gliclazide (Diamicron), available in Great Britain and Australia. Although many newer medications are receiving a lot of attention in the media, sulfonylureas remain among the most widely prescribed diabetes medications on the market. Dr. Steve Parker wrote a nice overview of sulfonylureas a few years back.
A few pertinent facts about the study referenced above:
I find this quite concerning, but I've only read the abstract and would like to read the entire study before commenting further. (If anyone is willing to share the full text with me, it would be much appreciated.) However, the well-known side effects of sulfonylureas are precisely what I saw in many patients in my former position as an outpatient dietitian in a large hospital:
Contrast these undesirable effects with those of metformin, a diabetes medication which is relatively safe, improves insulin sensitivity, decreases hepatic glucose output, and doesn't result in hypoglycemia or weight gain.
A very important point is that sulfonylureas are only used to cover postprandial blood glucose in response to a carbohydrate-containing meal. If minimal carbohydrate is consumed, sulfonylureas aren't necessary and can definitely cause hypoglycemia. So someone following a very-low-carbohydrate diet would need to discontinue sulfonylurea treatment but might continue taking metformin indefinitely, depending on fasting and postprandial blood glucose levels.
I realize most dietitians and diabetes educators advise people with type 2 diabetes that they should consume the same foods as everyone else and take insulin or insulin-stimulating medications to control the inevitable postmeal rise in blood glucose. But with all of the side effects listed above -- and now a potential increase in CHD risk -- I think that's a very misguided approach. It also places a large burden on the beta cells of the pancreas and may increase the rate of disease progression. Let's compare the risks of these medications to carbohydrate restriction for diabetes control. As long as the diet contains ample protein, healthy fat, plenty of vegetables, and smaller amounts of slow-digesting carbs from foods like nuts and berries, there are essentially no adverse effects than perhaps constipation, which is easily treated. And the benefits of low-carbing for someone with diabetes? No risk of hypoglycemia, increased satiety, and easier weight loss -- exactly the opposite of eating a "normal" amount of carbohydrates and taking sulfonylureas or insulin for coverage.
At the Low Carb Down Under conference in Melbourne at the end of September, I said that being respectful and courteous is the best way to convince dietitians and diabetes educators to recognize the benefits of carbohydrate restriction, and I stand by that statement. Remember, up until a few years ago I was one of those dietitians who promoted a low-fat diet with plenty of whole grains. But as we continue to find out about the drawbacks of various diabetes medications -- including several of the newer ones -- I understand people's frustration at being told they're a necessary part of diabetes management instead of being presented with an alternative solution. Since you're reading this, I hope you're someone who has benefitted from a low-carbohydrate lifestyle or would like to. The best that we can do is to continue speaking out and sharing our experiences, knowing that the evidence is on our side and at some point most health professionals will understand that carbohydrate restriction is the best and safest option.
1. Li Y, et al. Sulfonylurea Use and Incident Cardiovascular Disease Among Patients With Type 2 Diabetes: Prospective Cohort Study Among Women. Diabetes Care 2014 Aug 22
2. Braatvedt GD, et al. The clinical course of patients with type 2 diabetes presenting to the hospital with sulfonyl-induced hypoglycemia.Diabetes Technol Ther 2014 Jul 10
3. Fonseca V, et al. Determinants of weight gain in the action to control cardiovascular risk in diabetes trial. Diabetes Care 2013 Aug;36(8):2162-8
4. Madiraju AK. Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. Nature 2014 Jun 26;510(7506):542-6
5. Feinman, et al. Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Nutrition 2014 July 16
A couple of days ago I received the August issue of Today's Dietitian and was excited to see "The Top 10 Diabetes Meal Patterns" on the cover. My excitement faded, however, when I realized that the list was the same one published by US News & World Report in January, which ranked the Atkins and Paleo diets 25 and 31, respectively. Still, I held out a glimmer of hope that something about the benefits of carbohydrate restriction for diabetes would be mentioned in this article. Unfortunately, that wasn't the case.
The author of the Today's Dietitian article reviewed the diets that made the Top 10 and included commentary by dietitians with expertise in diabetes management. With the exception of Dr. Andrew Weil's Anti-Inflammatory Diet and the Mediterranean Diet, all of the plans are low to very low in fat, and none are low in carbohydrates. The dietitians discussing the diets in the article seem to think that calories are more important than carbohydrates because "people with diabetes and prediabetes typically require weight loss." Perhaps that's why a Academy of Nutrition and Dietetics spokesperson gave high marks to the No.1 ranked Biggest Loser diet, which limits calories to 1200 per day and encourages vigorous exercise. I have several issues with the Biggest Loser approach to weight loss that will have to wait for another day, but for now I'll say that almost everyone with diabetes will get hungry eating a low-fat, high-carbohydrate diet that contains 1200 calories (I certainly would), so they're unlikely to stick to it for any length of time. In addition, not all people with diabetes or prediabetes require weight loss, and many will struggle to achieve adequate glycemic control eating 50+ grams of carbohydrate at every meal. And although it appears that the diets are being discussed in terms of their effectiveness for type 2 diabetes rather than type 1, this should have been clarified.
Several of the plans are plant-based: Engine 2, Flexitarian, Ornish, and Vegetarian. There is some positive research on plant-based diets for diabetes management, so I understand the inclusion of these diets here. If people with diabetes want to follow some form of vegan or vegetarian diet, that's certainly their right. But others will find it difficult to adhere to the diet. There are many studies supporting carbohydrate-restriction for diabetes as well, and it deserves a mention somewhere in the Today's Dietitian article. Perhaps after the following quote:
"Every year since 2010, US News & World Report has ranked the year’s most popular diets. Using a panel of experts, including RDs and physicians specializing in diabetes, heart health, and weight loss, diets are ranked in eight categories, such as diabetes and heart disease prevention and control, as well as easiness to follow and likelihood of weight loss. According to the 2013 ADA nutrition recommendations, there are several meal patterns that have shown good results in people with diabetes."
Or even better, after this one:
"The 2013 ADA nutrition recommendations show that the quantity and type of carbohydrate in food impacts blood glucose levels, and the total amount of carbohydrate eaten is the primary predictor of glycemic response."
I realize that acceptance of low-carbohydrate diets is difficult for many dietitians, but a it is listed in that ADA paper (page 6) as an option. I've written a few journal and magazine articles about the benefits of carbohydrate restriction for diabetes (listed on my About Me page), and last August Today's Dietitian published an excellent article on this subject authored by my friend and fellow dietitian Aglaee Jacob. We're not advocating anything extreme; we both believe in a whole-foods-based approach with a flexible range of carbohydrate intake based on personal tolerance, preferences, and goals. I'm going to be speaking about carb restriction for diabetes at the Low Carb Down Under conference in Melbourne later this month, and it's going to be great to meet another low-carb dietitian who's presenting at the event, Dr. Caryn Zinn from New Zealand, along with the other speakers. I'm also very encouraged by the number of dietitians I've been in contact with over the past couple of years who support a low-carbohydrate lifestyle for people with diabetes or are at least open to the idea.
The American Diabetes Association has taken a big step in the right direction by recognizing carb restriction as an option for the millions of people who struggle with this often devastating disease, and I'm hopeful that more dietitians will come around to realizing how effective and sustainable this way of eating can be before it's time to rank diets for US News & World Report's 2015 list.
A couple of days ago I received an email from the makers of a soy-based protein bar that began:
"Scientific research continues to show that a plant-based diet is a healthy dietary pattern. In fact, previous versions of the Dietary Guidelines for Americans have emphasized plant-based diets, and the 2015 Dietary Guidelines Advisory Committee appears to be supporting these previous conclusions."
I'd heard this before, after the US Dietary Guidelines Advisory Committee (DGAC) held their third public meeting on the subject this past May. The fourth meeting is scheduled to be held on the 17th and 18th of July, and there's an opportunity to participate online, if you're interested.
It does seem that plant-based diets -- which are usually, although not always, synonymous with vegetarian or vegan diets -- are gaining favor in terms of public perception of their health benefits and sustainability. While I value the contribution vegetables, fruits, and nuts make to our diet, I disagree that most people would benefit from adopting a diet consisting solely of plant foods and have written about this before. And I'm disappointed that low-carbohydrate diets aren't being presented as an alternative at this point, particularly for the many groups of people who would benefit from them.
However, I dislike the confrontational and accusatory messages I've seen from many advocates on both sides in blog posts, comments, and social media sites. I'm passionate about carbohydrate restriction (apparently I'm not supposed to use this phrase to describe myself, but I think it fits), and I get upset when people criticize it and make claims about the superiority of plant-based diets too. But in my opinion, being respectful of the other side -- who are often equally committed to their way of eating -- while letting the evidence in favor of low-carbohydrate diets speak for itself, is the best way to go.
You may have already seen the debate between Dr. Eric Westman and Dr. T Colin Campbell held at the University of Alabama held in the spring of 2013. Both of these men have put many years into researching the effect of diet on various aspects of health. Each strongly believes that his way is the healthiest and most sustainable even though they are quite different. Dr. Campbell's view is that a plant-based, low-protein, low-fat, high-carbohydrate diet provides optimal nutrition, while Dr. Westman favors an eating plan that is very low in carbohydrate, moderate in protein, and high in fat. I encourage you to watch the video if you haven't already, or even if you have. Notice how Dr. Westman seeks to find common ground with statements like "There's more than one way to achieve excellent health," and then goes on to present the large body of evidence --including randomized clinical trials -- supporting carbohydrate restriction for diabetes, metabolic syndrome, and obesity, with early but promising research on ketogenic diets for cancer and neurological disease. I strongly agree with this approach and feel it's what will ultimately allow for more flexibility in the Dietary Guidelines -- specifically, including low-carbohydrate diets as an option.
I'd like to preface this blog post by apologizing for its length, including links to several long articles. Also, for anyone who doesn't know me, I'm a vocal and enthusiastic supporter of low-carbohydrate diets, but I always strive to be balanced in my writing. I'm very nonconfrontational and don't like "getting into it" with people who disagree with me. However, I expect I'll receive plenty of negative feedback from this article because of the controversial topic.
Cholesterol Results From June 2013 through November 2013
My cholesterol levels have always been higher than average. LDL has ranged from 120s-150s as far back as I can remember, long before I began following a moderately carbohydrate-restricted diet back in 2011. In June of last year, I reported my NMR (Nuclear Magnetic Resonance) LipoProfile results after almost a year of consuming a very-low-carb ketogenic diet (VLCKD) containing less than 50 grams net carb per day. I was very happy with these values and frankly a little surprised that I achieved them while eating delicious, satiating foods.
Lipid Profile from November 2013
In November of last year, I had a standard lipid profile done as part of lab work for my annual physical:
Total Cholesterol: 300
My numbers had increased, but I wasn't terribly concerned about the LDL-C, since on a few occasions it had been nearly that high in the past. Seeing a total cholesterol of 300 was a bit troubling, but I knew it was partially due to having extremely high HDL (Apparently high levels of some types of HDL can also be problematic, although I didn't realize this at the time). Looking back, although I wasn't tracking my intake online regularly back then, I'm pretty sure I was eating the same or perhaps a little more fat than when I had the NMR done five months earlier.
Nutritional Ketosis Experiment
At the beginning of January, I decided to experiment with lowering my carb intake further in order to achieve nutritional ketosis. I didn't want or need to lose weight, but after speaking with a few people who'd reported improved mental focus and energy on minimal carbs and ketone levels between 1.5-3.0, I was intrigued. For the record, I felt great prior to this experiment: no symptoms of adrenal fatigue, excellent blood sugar control, lots of energy, good sleep, etc. But was there a possibility I could feel even better in deep ketosis? I'm a curious type, so I decided to try it for a few months. I had a ketone meter but didn't test very often because the strips are ridiculously expensive. But when I did check prior to this experiment (first thing in the morning, the only time I've ever tested), my ketones ranged between 0.4-1.0 mm.
I began tracking my intake on My Fitness Pal, as many of my clients were doing. I lowered my net carbs to roughly 20 grams per day, although total carbs were often still around 50 grams because I ate a lot of avocados, unsweetened cocoa powder, and high-fiber vegetables like cauliflower. However, my consumption of berries dropped from 1-1.5 cups per day to 5 or 6 every morning at breakfast. I tried to keep protein around 70-80 grams daily (I'm 5'8" and 125 lbs, so this isn't all that low), and I ate more fat in order to maintain rather than lose weight. I never drank bulletproof coffee or added lots of butter or coconut oil to my food. But I did eat a fair amount of cheese, cream cheese, ricotta, and moscarpone, and I began using heavy cream instead of half-and-half in my coffee and tea. I still ate vegetables at every meal, although smaller amounts.
I tested blood ketones a couple of times a week in the morning, and results ranged from 1.2-1.8. After 3 months of eating this way, in all honesty, I didn't feel any different. I still felt great, slept great, etc., but I can't say I had more energy or experienced any cognitive benefits. My weight stayed the same, and my blood sugar control remained good. However, my lipids had definitely changed, and not for the better.
Cholesterol Results from April 2014
I had an NMR drawn at the end of April, and this time I'll admit to being more than a little upset when I saw the results:
I ordered this NMR through a different lab, so there are a few additional labs (mainly VLDL related) that weren't included in the one from June of 2013.
I was really surprised by how much my cholesterol had gone up since the prior test. My first thought was that perhaps my thyroid levels were off. (I have hypothyroidism that was diagnosed shortly before I went low carb, but my levels have been stable for the past few years on desiccated thyroid). However, I didn't feel at all hypothyroid and wasn't scheduled to have my thyroid labs re-checked until summer.
"Why Are You Concerned When You Have Such High HDL-C, Low Triglycerides, and Large, Fluffy LDL-C?"
While I've always been comfortable with higher than ideal cholesterol levels, having an LDL-C over 200 is a different story. The highest value I'd ever seen prior to last December was 158, I believe, about eight years or so ago when I was still following a low-fat, high-carbohydrate diet. But as far back as I can remember, my LDL-C was in the mid 120s to 150s regardless of what I ate, and my total cholesterol was never more than 260. My first NMR was the one last year, so I don't know what my LDL-P values were prior to 2013, but I'm assuming they were above the optimal range, although likely not over 1600. You can see that my LDL and total cholesterol each went up about 100 points and my LDL-P increased by 700 points in a 10-month period. My triglycerides even went up somewhat, although 60 is still pretty low. Although it's my understanding that LDL-C in an NMR is measured directly rather than by using the Friedewald equation (maybe a lipid expert can confirm this), when I plugged my numbers into an online calculator that estimates LDL-C, I got exactly the same number as in the NMR report, 221, for the Friedewald equation and 182 for the Iranian formula (The Iranian formula is believed to be more accurate when triglycerides are over 400 or less than 100).
You may be wondering what LDL-P is, since it's not reported in a standard lipoprotein profile and most doctors don't order it. Dr. Axel Sigurdsson does a great job explaining everything you ever wanted to know about it in his post about LDL-P, but I'll try to give a quick summary. LDL-P is a measurement of the number of LDL (low-density lipoprotein) particles in your blood which carry cholesterol, triglycerides, and another type of fat called phospholipids. According to lipidologists (experts in the field of cholesterol and other lipids), LDL-P is the strongest predictor of risk for cardiovascular disease (CVD) and future cardiac events. Total cholesterol greater than 300 and LDL-C greater than 190 are also associated with significant CVD risk. High levels of LDL-C are prone to oxidation, and oxidized LDL has been linked to the development of arterial plaque and coronary artery disease (CAD). Sometimes people have normal LDL-C and high LDL-P or vice versa (the term for this is discordance), but most people with very high LDL-C have high LDL-P as well. These findings are from recent studies, not decades-old research reported by Ancel Keys.
I want to make it clear that this type of dramatic elevation in LDL-C and LDL-P doesn't occur in most people who adopt a very-low-carb, high-fat diet. I've seen estimates that somewhere between one quarter and one third of low-carbers experience this. I've met and read about several who have. Most people who eat VLCKDs see their cholesterol rise only slightly, not at all, or even decrease, remaining within or near the normal range. I've met plenty of folks like this as well. I've also spoken with people who tell me their LDL cholesterol has always been over 200 and didn't really change after switching to a VLCKD. This is in sharp contrast to what happened to me: going from relatively stable LDL-C between 120s-150s to 221 within a very short period of time.
Of course, many things can affect a person's cholesterol levels, including stress, illness, and injury. Aside from familial hyperlipidemia (FH), there are other genetic disorders of lipid metabolism. Some people's livers produce large amounts of cholesterol (hyper secretors), while others absorb a lot of cholesterol from food (hyper absorbers), and some have both of these issues. My past lipid profiles didn't suggest FH, and I haven't been tested to see whether I have increased hepatic cholesterol production or increased intestinal absorption. I assume I'm probably a hyper secretor, since my levels were higher than average even during my 10 years as a low-fat vegetarian who ate a lot of egg whites but very few yolks or other cholesterol-containing foods.
I do have a family history of heart disease on both sides. My maternal grandfather suffered four heart attacks (the last one fatal), and my maternal grandmother also had coronary artery disease (CAD). My dad's brother has had two heart attacks, and his mother had CVD and died of a stroke. My mom has been on statin therapy since she was diagnosed with CAD ten years ago. (I'm not going to debate the risks vs. benefits of statin therapy in this post, but I'm not a big fan except in certain instances.) You may be wondering what kind of diet my relatives followed. Given that they all grew up and spent their entire lives in Switzerland (with the exception of my mom, who immigrated to the US at age 19), they obviously weren't following the Standard American Diet, but they weren't low-carbers either. My grandfather smoked and had diabetes, and my mom smoked for many years, but my other relatives didn't, and all were moderately active. I've never had a calcium scan or a carotid-intima thickness test(CIMT) to check for atherosclerosis but am looking into having these done. Even if they show no disease at this point, my goal is obviously preventing CAD, heart attack, and stroke in the future.
My NMR results indicate I have the large, pattern A type of LDL with a low number of the more atherogenic small LDL particles (small LDL-P). This is definitely a good thing. However, although I've heard large, fluffy LDL characterized as "harmless" and even "protective," I'm having trouble finding convincing evidence supporting this assertion, especially in the setting of cholesterol levels as markedly elevated as mine. In fact, the authors of the Multi-Ethnic Study of Atherosclerosis (MESA) study summed up their findings as follows:
"Contrary to current opinion, both small and large LDL were significantly associated with subclinical atherosclerosis independent of each other, traditional lipids, and established risk factors, with no association between LDL size and atherosclerosis after accounting for the concentrations of the two subclasses."
Subclinical atherosclerosis is the period when changes are happening in the arteries but the hallmarks of atherosclerosis (i.e., plaque and fatty streaks) haven't developed to the point where the disease can be diagnosed.
It's been pointed out that no studies have been conducted on people following VLCKDs who have very high LDL-C and LDL-P levels, and that's certainly fair to say. However, according to many MDs with expertise and/or personal experience in this area, we really don't know whether CVD risk is lower in low-carbers with cholesterol elevations of this magnitude.
What Do The Experts Say About Very High LDL-C and LDL-P?
I studied lipid metabolism in college as part of the coursework required to become a registered dietitian, but I'll be the first to admit that I have no expertise in that area. I think it's important to listen to the experts in this field since they best understand all of its complexities, including the genetic variations that influence cholesterol levels and the development of CAD. Keep in mind that the physicians listed below are all advocates of carbohydrate restriction to some degree.
Dr. James Underberg is a lipidologist and hypertension specialist in New York City who told me that he has seen similar dramatic increases in total and LDL cholesterol in some of his patients following a carbohydrate-restricted diet. One of the interventions he recommends in these cases is replacing a portion of dietary saturated fat with monounsaturated and polyunsaturated fat sources.
Although technically not a lipid expert, Dr. Rakesh "Rocky" Patel is very familiar with current lipid research as a family doctor in Arizona with hyperlipidemia who treats many people with diabetes and metabolic syndrome. He recommends the CarbNite (cyclical low-carb) method for most of his patients and also follows this approach himself. Back in the fall of 2012, he wrote a fantastic blog post entitled Does LDL-P Matter? in which he described improvement in his carotid intima thickness despite a significant increase in LDL-C and LDL-P after switching to a carbohydrate-restricted diet. When I received my NMR results from April, I asked him if we've learned any more about very high lipids in the context of a VLCKD since he wrote that piece. He responded:
"Not really. It really is an understudied issue. Unfortunately, all the trials in the literature involve the Standard American Diet. Really, I think that before we engage in any discussion regarding cholesterol, one has to establish if atherosclerosis is present in any form. So using testing like CT calcium scoring, carotid intimal thickness testing (CIMT), and genomic scoring (Corus CAD, Cardiodx) becomes imperative and certainly provides context to the lipids."
Dr. Axel Sigurdsson is a cardiologist who practices at a large university hospital as well as a private heart clinic in Iceland. In my opinion, his Doc's Opinion blog provides some of the most balanced, easily understood information about lipids and cardiovascular disease online. I described my experience to him and asked for his thoughts. His response:
"I've seen this lipid response (a very high jump in LDL-C and LDL-P) a number of times in individuals who adopt a low carb/ketogenic diet with relatively high amounts of saturated fat. It seems that a certain percentage of people react in this way. In fact, the lipid response to this type of diet may be genetically determined. Of course, we know that high LDL-C and LDL-P are associated with increased risk of CHD (coronary heart disease). However, nobody really knows what it means in this metabolic situation (nutritional ketosis) and to what degree it is associated with increased risk. Some claim it's not, but I think the evidence is lacking for such a conclusion. On the other hand, we also know that many people with high LDL-C and high LDL-P never have CHD. Of course, you may be one of those people. However, it is difficult to ignore altogether the possibility that high LDL-C and LDL-P may increase the risk of atherosclerotic problems."
Lipidologist Dr. Thomas Dayspring wrote an excellent article about a woman who had an experience similar to mine on a low-carb, high-fat diet, although her case involved weight loss as well. The article is available from his Lecture Pad series, and I highly recommend reading it in its entirety. (You'll have to register to view it, but registration is free). Although it may not always seem like it, he's actually quite supportive of carbohydrate restriction, particularly for people with metabolic syndrome. I didn't discuss my case with him, but here are two quotes from that article:
"We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C)."
"Could the low-carb crowd be outliers and in them we can ignore LDL-C and LDL-P? The advocates of those diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is that there is no data anywhere that shows they are an exception. Their belief is that by reducing all other atherosclerotic risk factors and normalizing their arterial wall and endothelial biology, that apoB-containing lipoproteins like LDL cannot enter the arterial wall. Although LDL-C and LDL-P in plasma are high, none of the cholesterol content of the apoB particles gains entry into the arterial wall. Is that plausible??? Sure! But is that also erroneous or wishful thinking? Sure? Does one want to bet their CV health or life on a plausible theory? Some do and some do not. Seems to me the first step is to do what this woman did: adjust the nutritional regimen."
He also states that when ketone bodies are present in excess, they can enter the cholesterol synthesis pathway, thereby increasing serum cholesterol levels.
While I agree with Dr. Dayspring on several issues, I disagree with his position (stated in another great article, Understanding the Entire Lipid Profile) that cholesterol-lowering medication is indicated for everyone with LDL-C greater than 190. I think nutritional intervention should be tried first, as it seems to be effective for at least a portion of people willing to do it.
Some of you may have seen spikes in cholesterol similar to mine after being on a low-carbohydrate, high-fat diet for a short period of time or possibly after a few years. You may not be that concerned, and I can understand that given the many positive effects LCHF can have on health, including certain cardiac risk factors. I also think there are still a lot of unanswered questions regarding the risk of elevated cholesterol in the setting of low insulin levels and optimal blood glucose control. But based on the evidence we do have, along with my strong family history of heart disease, I just wasn't comfortable with my numbers. And although I haven't seen this happen in any of my clients yet, I'd definitely recommend some sort of dietary intervention for them if it occurs in the future.
Dietary Changes and NMR Results from June 2014
Over the past two months I made a few small but significant changes to my diet in an effort to lower my cholesterol levels:
1. I cut back on saturated fat, particularly dairy fat and coconut oil, which contain the types of saturated fatty acids with the greatest potential to raise cholesterol.
2. I increased protein back to my previous intake of about 100 grams per day.
3. I doubled my net carb intake from 20 grams to 35-45 grams per day.
4. I began having chia seeds almost every day.
5. I ate sardines 4-5 times a week.
I still eat plenty of saturated fat, including some dairy fat. I drink coffee and tea with half-and-half (only 1 gram of carb in 2 Tbsp), always order Insalate Caprese made with fresh mozzarella at Italian restaurants, and continue to eat eggs cooked in a little butter for breakfast every other day. I still have burrata, ricotta, and moscarpone occasionally and continue eating red meat about 3 times a week. My total fat intake now ranges from roughly 80-100 grams per day, which is about 50-65% of my total caloric intake. That's still a LCHF diet! And in my case, it's also a mildly ketogenic one, since when I've checked my ketones in the morning (again, I only do this sporadically), they've been 0.4-0.8. Personally, I don't see the need to be in ketosis for my own health; to control my blood glucose, I eat a low-carb diet which just happens to be ketogenic. My weight hasn't changed (which was my goal), energy levels are good, sleep is excellent, etc.
I just received my new NMR results from labs drawn earlier this week:
My LDL-P and LDL-C are still higher than I'd like, but they've dropped considerably in a short period of time. I'm especially impressed by the 44-point drop in my LDL-C. My HDL decreased a bit as well but is still quite high. Considering this occurred in less than two months, I'm pretty happy with these results and hope they continue to improve until they return to the "Above Optimal" to "Borderline" ranges, which I consider normal for me.
As I said at the beginning, I'm a strong proponent of a low-carbohydrate lifestyle. I don't think that's ever going to change. But I feel it's important to look beyond the benefits and address the changes in lipids some people experience that could potentially have adverse effects. This was an n=1 experiment, of course. Remember, most people won't experience extremely high cholesterol levels on a VLCKD. But for me and others who do, I don't believe in shrugging it off and dismissing the results of studies because their subjects weren't following a carb-restricted diet. As a dietitian, I just can't say, "Go ahead and eat as much butter, cream, and bacon as you want. It doesn't matter how high your LDL-C and LDL-P are as long as you're eating low carb and your other markers are low," even if that's what many want to hear. Because we just don't know at this point. Maybe one day there will be evidence demonstrating that VLCKDs are cardioprotective even in the setting of significant hyperlipidemia. I truly hope that's the case. But in the meantime, I'm going to eat a low-carb diet that keeps my lipids in a range I feel more comfortable with.
***UPDATE: Recent NMR results, cardiovascular disease risk and what I eat
1. Otvos JD, et al. Clinical Implications of Discordance Between LDL Cholesterol and LDL Particle Number. J Clin Lipidol. 2011 Mar-Apr;5(2):105-13
2. El Harchaoui K, et al. Value of low-density lipoprotein particle number and size as predictors of coronary artery disease in apparently healthy men and women: the EPIC-Norfolk Prospective Population Study. J Am Coll Cardiol. 2007 Feb 6;49(5):547-53
3. Cromwell WC, et al. LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study - Implications for LDL Management J Clin Lipidol. 2007 Dec;1(6):583-92
4. Mora S, et al. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2007 May;192(1):
5. Waterworth DM, et al. Genetic variants influencing circulating lipid levels and risk of coronary artery disease. Arterioscler Thromb Vasc Biol. 2010 Nov;30(11):2264-76
6. Moriel P, et al. Lipid peroxidation and antioxidants in hyperlipidemia and hypertension. Biol Res. 2000;33(2):105-12
7. Ohlsson L. Dairy products and plasma cholesterol levels. Food Nutr Res. 2010 Aug 19;54
8. Mensink RP, et al. Dietary saturated and trans fatty acids and lipoprotein metabolism. Ann Med. 1994 Dec;26(6):461-4
I'm a firm believer in keeping track of the foods you eat and the nutrition they provide. Many times people believe they're doing everything right but find that their weight, ketones, and blood glucose levels tell a different story. Online tracking apps like My Fitness Pal are helpful, but they weren't designed for people following a low-carbohydrate or ketogenic diet. However, there is an app created specifically for us: KetoDiet App. Some of you may be familiar with Martina's KetoDiet App website, including the blog, which contains fantastic recipes and useful information about healthy, low-carb living.
I love the look and functionality of this app. First of all, it's highly customizable based on your goals for carb intake and weight loss. There are currently over 100 recipes that are beautifully photographed through every step of preparation, and the instructions are very easy to follow. An RSS feed automatically adds new recipes that Martina posts to the website. The app allows you to easily enter your own foods, recipes, and restaurant items, in addition to the KetoDiet recipes. As you add items for the day, the energy (calories), protein, fat, fiber, and electrolytes are tabulated, along with net carbs, which are highlighted in green at the right edge. If you go over your personalized net carb goal (i.e., 30 grams), the color changes from green to red, instantly alerting you. Although the app is called KetoDiet App, you don't necessarily have to be on a ketogenic diet to use it, since you can program in whatever level of carb intake you like.
In my opinion, just about everyone on a low-carb diet would enjoy using this app because of its innovative design, ease of use, reliability, and comprehensive list of mouth-watering recipes. Those of you who read my blog regularly know that I like to be balanced and consider both the positive and negative aspect of everything, but in all honesty, I can't find anything negative to say about this app. I think it's fantastic and, along with the KetoDietApp for iPhone and KetoDietApp book, an excellent value. (Note: The iPhone app is a basic version which does not include the planner and tracker.)
If you haven't already, I highly recommend checking out the KetoDiet App blog and trying out some of the recipes, such as Paleo Greek Meatballs (Soutzoukakia), Cajun Chicken Tacos, and Low Carb Strawberry and Rhubarb Panna Cotta.
Disclosure: Martina provided me with a free copy of KetoDiet App for iPad, but I have received no monetary or other compensation for this review.
Have you ever cut calories drastically in an attempt to lose weight quickly? I did that repeatedly in my teens, and it never turned out well; I felt hungry and miserable while I was dieting and ended up gaining back all the weight I lost because my appetite was out of control. The promise of rapid weight loss is enticing, particularly for people who have a significant amount to lose. But are the consequences worth it?
In a recent small study that hasn't yet been published, researchers from the Netherlands looked at body composition changes in people losing weight rapidly on a 500-calorie diet for 5 weeks vs. more gradually on a 1250-calorie diet for 12 weeks. Of the roughly 19 lbs lost on average between both groups, at the end of the study, the 500-calorie group had lost almost 3 times as much lean muscle mass as the 1250-calorie group (3.5 lbs vs. 1.3 lbs, respectively). This isn't surprising, since when caloric needs aren't being met, the body uses protein for energy, and muscle mass is broken down to provide amino acids that are essential for survival. After 4 weeks, the numbers looked a little better, which the study authors attribute to improved hydration and glycogen repletion (No mention of how much water weight was regained), but the 500-calorie group was still down about 2 lbs of muscle mass from where they started.
The results of this study made me think about the very-low-calorie HCG diet, which people follow for 3 to 6 weeks at a time, often in several rounds. First popularized in the 1950's by British endocrinologist ATW Simeons, the diet protocol involves taking injections containing HCG, human chorionic gonadotropin -- a hormone produced by pregnant women and approved for use as a fertility treatment -- and restricting calories to 500 per day. (There are also HCG drops, but apparently they contain negligible quantities of the hormone). HCG purportedly has appetite-supressant properties that make subsisting on such low energy intake bearable, and although studies suggest otherwise, many proponents claim it also increases fat burning and weight loss. The HCG diet fell out of favor years ago when researchers reported that the dramatic weight loss of up to a pound a day was due to starvation-level caloric intake rather than the hormone injections. However, within the past few years, there has been a resurgence in its use (thanks in part to the diet being featured on the Dr. Oz show), particularly among anti-aging doctors.
The HCG Diet: The Basics
In addition to containing very few calories, the HCG diet is extremely low in fat. The original HCG diet menu below specified the following menu every day, although some updated versions allow people to move some of the foods around to different meals:
Tea or coffee in any quantity without sugar. Only one tablespoon of milk allowed in 24 hours. Saccharin or stevia may be used.
1. 100 grams of veal, beef, chicken breast, fresh white fish, lobster, crab, or shrimp. All visible fat must be carefully removed before cooking, and the meat must be weighed raw. It must be boiled or grilled without additional fat. Salmon, eel, tuna, herring, dried or pickled fish are not allowed. The chicken breast must be removed from the bird.
2. One type of vegetable only to be chosen from the following: spinach, chard, chicory, beet-greens, green salad, tomatoes, celery, fennel, onions, red radishes, cucumbers, asparagus, cabbage.
3. One breadstick (grissino) or one Melba toast.
4. An apple, orange, or a handful of strawberries or one-half grapefruit.
The same four choices as lunch (above).
This is what dieters are instructed to eat for 4 weeks straight while undergoing HCG injections. Not much to look forward to at mealtimes, which is probably by design in order to prevent overindulging. Characterizing the diet as unappetizing would be an understatement.
The plan provides roughly 55 grams protein, 50 grams carbohydrate, and 9 grams fat. So the macronutrient percentages are about 44% protein, 40% carbohydrate, and 16% fat. 44% of calories from protein sounds like a lot but isn't in this case, and when calories restricted to 500, the protein will be used for energy rather than preservation of muscle mass anyway. After a 6-week break from the diet (I couldn't find any specific dietary guidelines to follow during this period), those who want to lose additional weight often resume the HCG injections and 500-calorie diet for another 4 to 6 weeks.
A Sustainable Alternative to HCG
Doctors recognize that loss of lean mass results in a lower resting metabolic rate. So why are many anti-aging physicians promoting a diet that will, if anything, accelerate the aging process by causing significant muscle loss and other health problems? Some claim that HCG allows people to burn their own body fat for fuel and prevent muscle breakdown, but there is no evidence for this. Studies going as far back as the 1970s indicate that the weight loss achieved on this diet is due to its very low calorie content rather than the HCG injections. (As an aside, I had to laugh at some of the "benefits" claimed on the HCG Doctors Directory site, such as "Improves one's singing voice." Really? And I would like to see clinical evidence that thyroid and adrenal function improve in people consuming 500 calories a day for weeks at a time.)
On the other hand, we have research suggesting that a carbohydrate-restricted diet with adequate calories and protein preserves muscle mass during weight loss, including an analysis of 87 studies that found greater fat loss and better retention of lean mass at lower carbohydrate and higher protein intakes. In addition, carb restriction tends to increase satiety, and most people report enjoying the diet and the wide variety of foods they can eat every day. Many experience rapid weight loss at the beginning, which typically slows down to a more gradual pace after the first week or two. Another benefit of a well-balanced low-carbohydrate way of eating is its suitability for long-term use, both for weight loss and maintenance.
I understand how difficult it is to lose weight and how rewarding it can be to lose rapidly. But it concerns me that there are doctors prescribing a diet so low in calories and nutrients along with hormone injections that were discredited years ago. Rather than encouraging immediate gratification with claims like "Lose up to 30 pounds in a month," why not recommend a sustainable way of eating that not only promotes safe weight loss but is highly pleasurable as well? Carbohydrate restriction has all of these things going for it, and more. In a nutshell, it doesn't feel like being on a diet, and that's one of the primary reasons it works well for so many people.
1. Stein MR, et al. Ineffectiveness of human chorionic gonadotropin in weight reduction: a double-blind study. Am J Clin Nutr. 1976 Sep;29(9):940-8.
2. Rabe T, et al. Risk-benefit analysis of a HCG 500-kcal reducing diet (cura romana) in females.
Geburtshilfe Frauenheilkd. 1987 May;47(5):297-307.
3. Lijesen GK, et al. The effect of human chorionic gonadotropin (HCG) in the treatment of obesity by means of the Simeons therapy: a criteria-based meta-analysis. Br J Clin Pharmacol Sep 1995; 40(3):237-243
4. Volek JS, et al. Comparison of energy-restricted very-low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutr Metab (Lond). 2004 Nov 8;1(1):13
5. Krieger JW, et al. Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression. Am J Clin Nutr 83: 260–274, 2006.
More Than Just a Risk Factor for Disease
The number of people with metabolic syndrome is increasing, yet those who have it often aren't aware of its significance. Originally identified as Syndrome X by Dr. Gerald Reaven in the 1980s, metabolic syndrome increases risk for cardiovascular disease, heart attack, stroke, and diabetes. It is diagnosed in people who have central obesity (waist circumference >35 inches in women or >40 inches in men) and meet at least two of the following criteria as set forth by the American Heart Association:
The majority of people with metabolic syndrome have prediabetes, defined as fasting blood glucose between 100-125 mg/dL and/or hemoglobin A1c between 5.7-6.4%. Interestingly, people with hypertension may have better overall glycemic control as a result of producing large amounts of insulin, but they often develop heart disease at higher rates because of persistent and significant hyperinsulinemia. Unfortunately, it's easier to dismiss concerns about you're health when you're told you "only" have prediabetes.
Insulin resistance is defined as the inability of cells to respond normally to insulin, resulting in higher blood glucose and insulin levels. It's the hallmark of metabolic syndrome. Recently it has been suggested that hyperinsulinemia may be what causes insulin resistance rather than the more commonly held view that insulin resistance leads to increased insulin output and subsequent hyperinsulinemia. Regardless of which occurs first, high levels of serum insulin result in elevated blood pressure, inflammation, and high triglycerides and VLDL cholesterol -- all of which increase the risk for vascular events, i.e., heart attack and stroke. Unfortunately, most people who are diagnosed with prediabetes or metabolic syndrome don't realize that they've already sustained damage. For instance, it's estimated that 50% of people already have heart disease at the time diabetes is diagnosed.
Lifestyle Goals: Is Standard Advice Helpful or Harmful?
The goals of treatment for metabolic syndrome are obvious: weight loss and improvement in blood pressure and lab values. Aside from drug therapy for lipids and blood pressure, what can be done from a nutritional standpoint? Here is the standard advice I found on many highly regarded websites, including the National Heart, Blood, and Lung Institute (NHBLI) site:
A typical recommendation is to achieve and maintain a BMI of <25, which may not be possible or even desirable for everyone, particularly muscular, large-framed men. The BMI is also meaningless for assessing abdominal girth and body fat vs. muscle. For instance, a man with a BMI of 28 with little body fat and a 32-inch waist is metabolically much healthier than a small-framed man with a BMI of 24, a 38-inch waist, and a considerable amount of visceral fat around his organs. Of course, in people with metabolic syndrome abdominal obesity is a given, but the goal should be decreasing waist circumference rather than BMI.
Follow a Heart-Healthy Diet
It really shouldn't surprise me at this point that the "heart-healthy diet" -- essentially the DASH diet -- so often advised for people with metabolic syndrome isn't the one I'd recommend. From the NHBLI website:
"Fill half your plate with fruits and vegetables. A healthy diet also includes whole grains, fat-free or low-fat dairy products, and protein foods, such as lean meats, poultry without skin, seafood, processed soy products, nuts, seeds, beans, and peas."
Yes, "processed" soy products.
So according to these recommendations, the following meal plan would be ideal:
Bowl of Raisin Bran cereal with sliced banana and skim milk
Turkey sandwich with low fat mayo on whole grain bread, orange
Yoplait Light yogurt with fruit
Tofu, rice, and vegetables with low-sodium teriyaki sauce
This advice is being given to individuals with metabolic syndrome, who by definition have insulin resistance and hyperinsulinemia with elevated triglycerides, low HDL, and/or impaired fasting glucose. Unless carbohydrate portions are kept very small and fat is added -- neither of which is recommended on a low-fat diet -- these guidelines are likely to exacerbate rather than improve biomarkers and weight. And, let's face it, this plan doesn't sound that appetizing or satiating and would be difficult to sustain for most people.
An Enticing Alternative: Carbohydrate Restriction
On the other hand, research has demonstrated that low-carbohydrate diets do the following:
Clearly, metabolic syndrome responds extremely well to carbohydrate restriction. Is there any other diet that has shown such impressive results? Some would argue that the Mediterranean Diet has demonstrated health benefits in this population, and there are certainly studies that support this claim. However, if large quantities of fruits, starchy vegetables, and grains are consumed, a Mediterranean diet plan can be as high in carbs as the low-fat plan listed above. Dr. Steve Parker has devised two Mediterranean-based diets that are appropriate for people with Metabolic Syndrome: the Low-Carb Mediterranean Diet and the Ketogenic Mediterranean Diet.
Here's an example of a low-carbohydrate meal plan based on Mediterranean Diet principles:
Greek yogurt with raspberries and chopped walnuts
Shrimp, tomatoes, and cucumbers with olive oil and basil
Mixed nuts or olives
Steak with grilled zucchini, mushrooms, and eggplant
Strawberries with whipped cream
I think that sounds like a pretty enjoyable and sustainable way of eating.
And yet in most papers, on most websites, and among most endocrinologists, carbohydrate restriction isn't even discussed as an option for metabolic syndrome. "Lose weight" seems to be the primary directive, and the recommendation for achieving this is typically a low-fat, low-sodium, high-carb approach. Interestingly, much of the research on hyperinsulinemia and insulin resistance over the past two decades has been published in Diabetes and Diabetes Care, which are journals of the American Diabetes Association, an organization which recently changed its position statement to include low-carbohydrate diets as an option for people with diabetes and prediabetes. I hope other organizations will follow their lead and begin promoting carbohydrate restriction as an option -- or better yet, the best option -- for those with metabolic syndrome.
1. Shanik MH, et al. Insulin resistance and hyperinsulinemia: Is hyperinsulinemia the cart or the horse? Diabetes Care 2008 Feb: 31 Suppl 2: S262-8
2. Reaven GM. Banting lecture 1988: Role of insulin resistance in human disease. Diabetes 1988 Dec;37(12); 1595-607
3. McGavock JM, et al. Cardiac steatosis in diabetes mellitus. Circulation 2007 Sep 4;116(10):1170-5
4. Winhofer Y, et al. Short-term hyperinsulinemia and hyperglycemia increase myocardial lipid content in normal subjects. Diabetes 2012 May;61(5):1210-1216
5. Volek JS, Feinman RD.Carbohydrate restriction improves features of the Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab(Lond) 2005 ;2:31
6. Castorini CM, et al. The effect of Mediterranean diet on metabolic syndrome and its components. J Am Coll Cardiol 2011 Mar 15:57(11)1299-313
Franziska Spritzler, RD, CDE