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.
Apo E4 and sterols: Lethal combination?

Apo E4 and sterols: Lethal combination?

11. February 2011 William Davis (24)
Phytosterols, or just "sterols" to its friends and neighbors, are a group of cholesterol-like compounds that are abundant in the plant world. Lately, however, sterols have proliferated in the processed food supply, thanks to the observation that sterols reduce LDL cholesterol when ingested by humans.

This must mean that sterols are good for you.

Uh oh. Wait a minute: There is a rare disease called sitosterolemia in which there is unimpeded intestinal absorption of all sterols ingested through diet. They must have really low LDL cholesterols! Nope. They develop coronary disease--heart attacks, angina, etc.--in their late teens and 20s. In other words, if sterols gain access to your bloodstream, they are bad. Very bad.

Conventional thinking is that only a modest quantity of dietary sterols gain access to the bloodstream. But there are two potentially fatal flaws in this overly simplistic line of thinking:

1) What happens when you load up your diet with "heart healthy" sterols, such as those in "heart healthy" margarines, mayonnaise, and yogurt, effectively increasing sterol intake 10-fold?

2) What happens in people with the genetic pattern, apo E4, that is carried by 25% of the general population that permits much greater intestinal absorption of sterols?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study
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Comments (24) -

  • Kathy Hall

    2/11/2011 12:04:41 AM |

    Does this include the beta sitosterol that is in most prostate supplements?

  • Lucy

    2/11/2011 12:32:16 AM |

    How can I get tested for sitosterolemia?

  • Anonymous

    2/11/2011 1:08:44 AM |

    I know for a fact that Costco sells 5000+ bottles of CholestOff every WEEK! The stuff is a blend of sterols.

  • preserve

    2/11/2011 1:43:45 AM |

    Yeah costco also has "sterol" oatmeal bars.

    I try to stick to the freezer and wine section.

  • Anonymous

    2/11/2011 2:46:10 AM |

    I like how you state plainly it's "rare," and now your followers are going to start to believe themselves to have this ailment. I like your blog, but as of late, you're war on heart disease is imitating the ad baculum aspects of America's war on terror.

  • Davide

    2/11/2011 3:04:46 AM |

    Excellent article. I've had the same exact thoughts and that's why I don't take supplementary plant sterols.

    It's pretty comical. When people supplement with sterols, all they are doing is swapping some of their cholesterol in LDL particles with sterols. The sterols essentially take the place of the cholesterol in the blood. But both have the proclivity to cause atherosclerosis.

    So, the cholesterol lowering effect is just an illusion.

  • Anonymous

    2/11/2011 4:16:23 AM |

    I'm not so sure Apo E4 would even be considered 'rare' amongst those who have heart disease problems... or who are considered high risk.

    E4/E4 is quite rare, but E3/E4 isn't really. I think it's around 25% of the population, if I recall correctly. And I'd expect amongst those with heart issues, it'd be higher than that.

  • Anonymous

    2/11/2011 7:56:33 AM |

    So what do you eat if you are disp. to Apo E4. If I eat sat. fat my LDP
    rocket up. If I eat more veg. and fruit and lean mead it rocket dovn.
    Am I on the track??

  • Dr. William Davis

    2/11/2011 12:40:05 PM |

    Hi, Kathy--

    Yes, it does.


    Lucy--

    In general, testing for sitosterolemia is not something I would recommend except in specific situations, in which case the various sterols in the blood can be measured.

    That was not the point of the discussion, but the far more common Apo E4 that affects 25% of the population, who thereby potentially hyperabsorb sterols.

  • Daniel A. Clinton, RN, BSN

    2/11/2011 3:46:49 PM |

    Ted,
    I can do you one better. This prospective cohort study (n=1137) found "Higher levels of HDL-C (>55 mg/dL) were associated with a decreased risk of both probable and possible AD and probable AD compared with lower HDL-C levels (hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03 and hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03). In addition, higher levels of total and non–HDL-C were associated with a decreased risk of AD in analyses adjusting for age, sex, education, ethnic group, and APOE e4 genotype." Here's the link to the abstract:  http://archneur.ama-assn.org/cgi/content/abstract/67/12/1491.
    Makes you wonder the REAL reason behind statin drugs.

  • Kevin

    2/11/2011 6:43:41 PM |

    I used beta-sitosterol for over a year.  I used it because I didn't want to take a 5-alpha reductase inhibitor such as Proscar.  But I developed the same side effects that Procar is known to cause:  Poor libido, gynecomastia and generalized muscle weakness.  I don't track cholesterol so I don't know what the beta-sit might have done to it.  Six months off the beta-sit and I'm just now starting to feel like a normal man again:  morning wood, etc.

  • Lucy

    2/11/2011 9:15:49 PM |

    That was my reason for asking... because I'm a 3/4

  • Anonymous

    2/12/2011 4:54:58 AM |

    Fructose Alters Brain Metabolism
    One of the competing theories to explain the obesity epidemic is a rise in fructose consumption causing alterations in hormone levels that increase appetite. UCSF med school prof Robert Lustig has a pretty good rant-lecture on the evils of fructose. Well, here's another study on part of the mechanism in the brain of how fructose might be causing increased obesity.

    PORTLAND, Ore. – The dietary concerns of too much fructose is well documented. High-fructose corn syrup has become the sweetener most commonly added to processed foods. Many dietary experts believe this increase directly correlates to the nation's growing obesity epidemic. Now, new research at Oregon Health & Science University demonstrates that the brain – which serves as a master control for body weight – reacts differently to fructose compared with another common sweetener, glucose. The research is published in the online edition of the journal Diabetes, Obesity and Metabolism and will appear in the March print edition.

    In humans the cortical brain control areas of the brain were inhibited by the influx of fructose.

    Functional MRI allows researchers to watch brain activity in real time. To conduct the research, nine normal-weight human study subjects were imaged as they received an infusion of fructose, glucose or a saline solution. When the resulting brain scans from these three groups were compared, the scientists observed distinct differences.

    Brain activity in the hypothalamus, one brain area involved in regulating food intake, was not affected by either fructose or glucose. However, activity in the cortical brain control areas showed the opposite response during infusions of the sugars. Activity in these areas was inhibited when fructose was given but activated during glucose infusion.

    This is an important finding because these control brain areas included sites that are thought to be important in determining how we respond to food taste, smells, and pictures, which the American public is bombarded with daily.

    The result increases the plausibility of fructose as a causal agent.

    "This study provides evidence in humans that fructose and glucose elicits opposite responses in the brain. It supports the animal research that shows similar findings and links fructose with obesity," added Purnell.

    If you want to reduce your weight also consider other theories for the cause of obesity including grains as a possible major cause.

    By Randall Parker 2011 February 09 05:42 PM  Brain Appetite

  • Dr. William Davis

    2/12/2011 4:57:38 PM |

    Hi, Peter--

    Thanks for catching that.

    Now fixed.

  • Might-o'chondri-AL

    2/12/2011 9:40:08 PM |

    Foods with naturaly occuring levels of Beta-sisterol: fruits like avocado, nuts like pecan & cashew, seeds like flax & pumpkin,
    legumes like soya & peanut, grains like wheat germ & rice bran, oils like corn & soy, plus herbs like Saw Palmetto & Pygeum. Once again it is good to recall that if something is good for you that doesn't automaticly mean more is better for you.

  • Gene K

    2/13/2011 7:29:32 PM |

    @Anon about naturally occurring sitosterol levels -

    As an APO E4 person, should I be concerned about my intake of avocado, flax seed, and tofu?

  • reikime

    2/13/2011 11:07:34 PM |

    couldn't leaky gut syndrome cause increased sterols in the bloodstream?

  • Anonymous

    2/14/2011 4:03:27 AM |

    So... how much sterols?
    For example almonds and other nuts are high in sterols. Lot of vegetables are high in sterols. In this blog nuts have been recommended often as well as a plant based diet. So does this change that?
    What should apoe4 people eat? They can't eat fat, now they can't eat vegetables? Is starving to death the only way to avoid heart disease?

  • Anonymous

    2/15/2011 7:12:55 AM |

    Also tofu and soy has been promoted which have esterols...

  • Kurt G. Harris MD

    2/16/2011 4:06:56 AM |

    Another benefit to total avoidance of plant oils!

    Miniscule n-6 means miniscule fat soluble sitosterols.

    Are you ready to advocate an animal-fat based diet for ApoE4 and the 45 total reported cases of sitosterolemia?

    If you worry about LDL, ApoE4 needs to be "low fat", but if you worry about early death and AD, I think high animal fat is the way to go for these folks.

  • Might-o'chondri-AL

    2/16/2011 5:42:19 PM |

    Isn't the problem for APOE4 the way the molecule degrades? Quite recently fish oil Omega 3 has been cited for allaying APOE4's side effects. The Omega 3 balances out the metabolite (an APOE4 protein fragment) that otherwise messes with the lipid structure of the mitochondria(s) membrane(s); it (fish oil) prevents dysfunction.

  • Janknitz

    8/24/2011 2:27:51 PM |

    http://m.npr.org/news/front/139889533

    I heard a report on this study on NPR yesterday.  It's important to note who sponsored the study in the first place.

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