Why obese people can't fast

9. September 2009 William Davis (21)
Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.
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Comments (21) -

  • Anonymous

    9/9/2009 12:21:40 AM |

    I agree with your post.
    Once you are adapted to a low carb diet Intermittant Fasting becomes really easy and you feel great without becoming hungry or mentally foggy. I wouldn't dream of trying IF on a high carb diet since it would be like self torture.

    Cheers
    GoEd

  • rfrancis

    9/9/2009 12:47:06 AM |

    Dr. Davis,

    I agree with you as far as this goes -- but I'd go a bit further.

    For those (myself included) who are substantially insulin resistant, and in particular type II diabetic, even years of a low carb diet may not beat the hunger cycle, very possibly (c.f. Gary Taubes and others) because that very insulin resistance interferes with the release of stored energy, ensuring that the insulin resistant person becomes hungry again every time they've exhausted (or worse, stored!) the energy obtained from their last meal.  Feelings of muscular tiredness, lethargy, even mysterious panic -- I doubt anyone chronically obese is strangers to some or all of these.

    Of course, even so, the first step is exactly as you say.  As for what comes next... I'm all ears. Smile  Personally, I'm trying to get my physician to at least investigate possible connections between subclinical hypothyroid and insulin resistance...

  • Stan (Heretic)

    9/9/2009 1:36:01 AM |

    Anonymous wrote: "Once you are adapted to a low carb diet Intermittent Fasting becomes really easy and you feel great without becoming hungry or mentally foggy."

    Absolutely!  On a high (animal) fat diet, our metabolism is identical to a fasting metabolism, therefore there is no noticeable change in feeling, stamina, not much hunger even after a couple of days!  There isn't much need to drink water either, since fat burning produces water.   Also we typically eat only one meal a day - that is completely sufficient without any need to snack.

    Stan

  • Ross

    9/9/2009 3:07:45 AM |

    Very similar to my own experience.  I used to try fasting, as my very liberal friends used to tell me that it's great for "purification" and "detoxification", but I couldn't hack it.

    Now I do a 36 hour "after dinner to before breakfast" fast about once a week (on random days of the week to shake things up) and the strongest symptom I have is during the afternoon and evening of the fasting day I get very mellow and relaxed.  I also feel small hunger pangs as I go to bed and that's about it.

  • Andrew

    9/9/2009 3:13:16 AM |

    gft chromium helps with fat metabolism

  • Rick

    9/9/2009 5:37:00 AM |

    Dr. Davis,
    Could you expand a bit on what you mean by the 2-hour cycle?

  • Lincoln

    9/9/2009 7:55:10 AM |

    This is a really good article which clearly explains the concept of the hunger cycle.  From my experience if people are particularly insulin resistance then a longer lead in time of gradually reducing carbs helps the body to adjust.  Then it is possible to include a period of fasting.

    Thanks

    Lincoln

  • Daddy

    9/9/2009 9:23:47 AM |

    I have only recently started in with the low carb diet.  I was curious if there is any knock against dairy too.  Thanks!

  • Methuselah

    9/9/2009 11:49:19 AM |

    Your article makes perfect sense, but the title is a little misleading. Clearly once an obese person has removed the 'unnatural appetite triggers' they will be able to fast as comfortably as a slender person who has eliminated those triggers. Indeed an obese person who has emiminated the triggers might be more able to fast than a slender person who has not.

  • Dr. William Davis

    9/9/2009 12:11:18 PM |

    Hi, Rick--

    After a carbohydrate load, blood sugar (glucose) increases sharply, followed by insulin. In response to insulin, blood sugar drops precipitously, often to levels below normal. This is where all the symptoms like mental fogginess develop.

    The entire cycle requires 90-120 minutes or so, depending on the foods consumed, the mix of foods and food types consumed, and individual responsiveness.

    Interestingly, of all foods, wheat triggers the fastest and highest glucose peaks, even compared to table sugar (sucrose).

  • Susan

    9/9/2009 1:03:31 PM |

    One thing you find when you go wheat-free (let alone low carb) is how difficult it is to buy anything for lunch that isn't wheat based. The great thing about IF is that it frees you from the endless repetition of "chicken caesar salad, please, hold the croutons and bacon bits." (Bacon bits are out because they're usually fake.) In fact, after a couple of days, you  can walk through a food court, and your only reaction is to marvel that all of these people are eating lunch, which is totally unnecessary. The other thing about IF is that it also makes it easier to say no to snacking or other mindless eating.

  • Anonymous

    9/9/2009 1:57:38 PM |

    I just want to know how all of you take your vitamins and other pills on an empty stomach?  I would vomit them right back up!

  • Gretchen

    9/9/2009 3:17:38 PM |

    It's not just "mental fogginess, fatigue, and insatiable hunger" that is the problem. When I was prediabetic and trying to lose weight, I had difficulty going on a diet because when I cut back on my food intake, I'd get what I now know are symptoms of hypoglycemia.

    I actually enjoyed being hungry, because it told me I was eating less than I needed.

    What I couldn't tolerate was "the shakes," accompanied by a feeling of panic that if I didn't eat immediately I'd die.

    Because many overweight people are also prediabetic, they probably have the same symptoms of hypoglycemia, caused by "too much insulin, too late."

  • PJNOIR

    9/11/2009 11:20:13 PM |

    As a former Fatty, I can understand the difficulties some would have with Intermittent fasting. Two points:  don’t start here. I managed to control my carb carvings first with Atkins, then was able to move on to Intermittent fasting when I was ready.
    Second- I don’t like that Ruth Frechman calls IF an “extreme strategy”- it just might be the healthiest Life Saver going.

  • Dr. William Davis

    9/12/2009 12:28:48 AM |

    PJ--

    I agree wholeheartedly.

    It shows how far our diets have drifted from the physiologic ideal when we have to shift away from it in steps!

  • PJ

    9/22/2009 2:41:42 PM |

    Um. I weigh about 380 and I have no trouble fasting. In fact it's 9:39am here on a Tuesday and the last time I ate was Sunday around 9pm. This is not because I was doing it on purpose (though I could retroactively assign some glorious reason to it I suppose), but because I'm painting my kitchen so making food was a pain in the butt and I didn't feel like it.

    However when I'm eating highcarb, going without food is horribly hard. The fact that I eat lowcarb is probably what makes it possible for me.

  • Matt Metzgar

    9/27/2009 6:19:05 PM |

    I agree completely with this.  If a person hasn't made the metabolic shift to fat-burning, then fasting will be painful.

  • trinkwasser

    10/2/2009 3:31:09 PM |

    Another "me too": my pattern was high BG at around 1 hour postprandial, returning to normal at two hours and dipping significantly below normal at three or more hours.

    This improved markedly with carb reduction, but I still needed to snack, until I started replacing those "heart healthy" Omega 6s with saturated fat.

    Getting the correct macronutrient balance *for me* lets me routinely go about six hours between eating, whatever my activity level, and those 14 hour fasts for blood tests don't have the response they used to cause.

    I'm still somewhat leery of fasting for that much longer though, as the resulting hypo symptoms and ensuing BG swings as my liver overcompensates are Not Nice and I don't want to push things so far that I restart this phenomenon

  • buy jeans

    11/3/2010 8:26:17 PM |

    Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

  • Jessica

    3/7/2012 6:56:48 PM |

    I''m fat.  I''m 245 lbs which is considered small on the morbidly obese scale, but still morbidly obese.  I have fasted a day at a time, every other day in prep for my 7 day trial.  I am starting my 7 day today.  Hopefully I don''t s**t the bed on this one.  I''m tired of being a fat ass, literally.

  • Gene K

    3/8/2012 7:20:10 PM |

    You may find the blog of Dr Jack Kruse useful, especially this post - http://jackkruse.com/my-leptin-prescription/. Definitely read all comments, and try to read as many of his other leptin-related posts as possible.

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To track small LDL, track blood sugar

24. December 2009 William Davis (28)
Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

21. December 2009 William Davis (0)
C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

17. December 2009 William Davis (36)
A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

16. December 2009 William Davis (0)
Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.