Almonds are the new wheat

Once you eliminate this genetically-altered Frankengrain called modern wheat, the diet should center around vegetables, nuts, healthy oils like olive and coconut, fish, meats, cheese, olives, avocados and other real whole foods. This is, in fact, the diet that I have advocated in my heart disease prevention practice, as well as my online program for prevention and reversal of heart disease.

But what if you'd like a piece of cheesecake or a nice slice of dessert bread---but you don't want to gain two pounds, spend 48 hours in the bathroom suffering with diarrhea and cramps, 3 weeks of joint pains and leg swelling, wade through mental "fog," anxiety, and rage just because you had that momentary indulgence---as you would with wheat?

That's why I've been focusing on recipes that allow you to have something familiar, e.g., chocolate coconut bread or biscotti, but using ingredients that will not generate the metabolic contortions triggered by wheat.

On perusing these recipes, you will notice that there are recurring ingredient themes. Many of the same ingredients pop up time and again. Among the most frequent, versatile, user-friendly, and tasty: Almonds.

You can use almonds as ground whole almonds, ground blanched almonds for a finer texture, ground roasted almonds, almond butter (though, for maximum health benefits, I prefer the ground whole almonds). Ground almonds allow you to recreate muffins, breads, scones, pizza crust, pie crust, biscotti, and cookies with health benefits that exceed that of whole wheat---but with none of the downside: no weight gain, no high blood sugar, no triggering of small LDL particles (#1 cause of heart disease in the U.S.), no accumulation of visceral fat, no appetite stimulation.

In short, you just have your chocolate almond biscotti or mocha cupcake and enjoy it, no health price to pay. So I call almonds the new wheat, except better.

Being regular is dangerous to your health

No, I'm not referring to your daily morning ritual in the bathroom. I'm talking about heart rate.

Counterintuitively, a perfectly regular heart rate is a marker of poor health. People with perfect regularity of heart rate have more heart attacks, for instance.

Regularity of heart rate occurs more commonly in people with hypertension and other metabolic derangements, and it signals increased risk for both heart attack and death. A perfectly regular heart rate, i.e., no variation in the time interval from beat to beat, suggests that the parasympathetic nervous system, the component of automatic ("autonomic") nervous system control that is associated with the relaxation response, feelings of well-being, quiet, and relaxation, is weak. It also means that the opposing sympathetic nervous sytem that regulates the "fight or flight," adrenaline-like response is allowed to be dominant. Dominance of the sympathetic over the parasympathetic system generates regularity of heart rate. Heart rate also tends to be faster, e.g., 85 beats per minutes rather than 55 or 60 beats per minute. So perfect regularity, as well as increased rate, is undesirable.

What we want is irregularity of heart rate. But not irregularity that occurs chaotically with no rhyme or reason. More precisely, we want variability in heart rate. And we want variability to occur in synchrony with breathing, i.e., the respiratory cycle.

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

Heart rate in healthy people typically varies 15-20 beats per minute within the respiratory cycle, e.g., 60 bpm at end-exhalation, 80 bpm at end-inspiration.

Restoration of increased heart rate variability is associated with reduced blood pressure, reduced blood sugars (HbA1c), reduced inflammatory markers and cortisol (associated with stress), even an increase in DHEA levels. Feelings of well-being and calm also develop.

Among the strategies to consider to restore heightened heart rate variability and slowed heart rate include:

--Omega-3 fatty acid supplementation
--Exercise
--Weight loss
--Deep breathing exercises
--Meditation, prayer, and biofeedback

For our Track Your Plaque purposes, we are folding in the HeartMath strategies, i.e., use of a heart rate monitor that calculates heart rate variability in the context of respiratory cycle. If you've not already done so, take a look at the two Special Reports devoted to this topic on the Track Your Plaque website.

You mean weight loss is hazardous to your health?

In my last Heart Scan Blog post, What is this wacky thing called weight loss?, I discussed how weight loss is associated with distortions in cholesterol and blood sugar values that can be very confusing, often leading your doctor to wrongly and unnecessarily prescribe drugs--since he/she likely rarely sees weight loss.

Blog reader, Donald K., posted his enlightening story:

I experienced this very thing.

After losing serious weight from the eliminating wheat, processed, and sugary foods (1 year in total) I lost 130 pounds. When I was nearly finished I went to see my doctor. He wanted to put me on statins. I explained to him how the data does not support application to me (no evidence of heart disease) and I got the mantra about standards of practice, etc, etc. I held my ground and decided I am much happier eating dairy, eggs, grass fed beef, wild caught fish, and as much raw foods (nuts, veggies, fruits) as my body desires to treat my health parameters.

Maintaining weight, it is easy. My BMI (23 down from 40) has remained constant for a few months now. You are right: metabolic processes definitely change. I no longer have sensations of glucose fluctuations or an uncontrolled appetite. I can only imagine the improved hormone regulation and metabolic communication going on inside my body.

The symptoms from obesity, all gone. Goodbye sleep apnea, hypertension, hemorrhoids, arrhythmias, gastroinestinal disruptions, smelly body, chaffing thighs, and others not mentioned. The positive effects are just as dramatic, but I don’t want to ramble on.

Weight loss? What is it? Getting your life back!


Brace yourself: If you are following the nutrition advice posted here and in the Track Your Plaque program, or the discussion I've initiated in Wheat Belly, then you may find yourself in the very same health predicament as Donald. Arm yourself to protect yourself against the drug-wielding ways of doctors. No, weight loss to achieve ideal weight is definitely not bad for health. But your doctor's misinterpretation of its effects can be!

What is this wacky thing called "weight loss"?

I've discussed this before, but it has proven such an (encouragingly!) frequent issue that I thought it was worth discussing once again.

What happens when you lose weight?

The process of weight loss is characterized by multiple shifts in metabolic patterns that can be confusing. To the uninitiated eye, weight loss can look like a disastrous distortion in metabolism. The naive doctor on seeing your lab values, for instance, might insist you take a statin drug, a fibrate like Tricor (to reduce triglycerides or increase HDL), or simply berate you for your bad health habits--when it's actually a good thing you've accomplished.

So when you lose weight, say, 30 pounds in 3 months, what have you accomplished?

Energy stored as fat, especially from visceral fat stores, is mobilized into the bloodstream. It floods the bloodstream as fatty acids and triglycerides. These fatty acids and triglycerides don't occur in isolation, but interact with other particles and metabolic patterns. The resulting blood patterns include:

--Increased triglycerides--An increase in triglycerides, for instance, from 90 mg/dl to 200 mg/dl in the midst of weight loss is common.

--Reduced HDL--The flood of triglycerides leads to increased degradation of HDL, thus a drop. A drop in HDL from, say, 40 mg/dl to 27 mg/dl--very frightening to people--is exceptionally common.

--Increased blood sugar--The flood of fatty acids and triglycerides results in insulin resistance, leading to higher blood sugars. It is not uncommon for someone with pre-diabetes to develop diabetic-range blood sugars, or a non-diabetic to show pre-diabetic blood sugars.

--Increased small LDL particles--Though small LDL is highly variable during weight loss. When it does happen, it's probably from the interaction of VLDL (triglycerides) with LDL particles and the reaction that overloads LDL particles with triglycerides and conversion to small LDL particles.

So why don't doctors often recognize these patterns when a patient loses weight? Because they rarely see it. Most of my colleagues are accustomed to having patients come back with weight gain, getting heavier and heavier each time. Lose weight? Impossible! So they just don't recognize weight loss effects when they see it. As followers of The Heart Scan Blog know, a frequent conversation around here is "Am I too skinny?" or "How do I stop losing weight?"

The solution: Be patient. Be patient and wait about two months after a weight plateau has been achieved. That's when the numbers "settle down" and you see marked drops in triglycerides, increases in HDL, drops in blood sugar, reductions in small LDL.

As with many things, it's all about timing.

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Even moore from Jimmy Moore

The ubiquitous and irrepressible Jimmy Moore posted even more commentary about the Wheat Belly phenomenon here, what he calls "The Wheat Belly Bonanza."

Is low-carb really, at its core, little more than elimination of wheat? Sure, corn, rice, and sugar exert deleterious effects. But the dominant effect--by far--is the elimination of wheat. So is the low-carb movement really, at its core, a wheat-elimination movement?

Food (non-wheat-containing, of course) for thought.

Heart Scans: An Interview with Jimmy Moore

My friend, Jimmy Moore, of The Livin' La Vida Low Carb Show, posted this video of an interview I did with him.

I provide some background on how heart scanning came about and how it led to the creation of the Track Your Plaque program.

It reminds me how far we've come over the 8 years since the program got started. From its modest start as just an information resource to help people understand their heart scan score, to a comprehensive program that helps followers gain incredible control over coronary plaque and coronary risk that has now expanded to over 30 countries. High-tech heart procedures still dominate public consciousness, but the tremendous power of real heart disease prevention efforts are gaining more and more attention as each day passes.

Wheat Belly #5 on New York Times Bestseller list!

The New York Times just released its bestseller list due for release September 18th, 2011 . . . .

Wheat Belly is #5!! (That darned Jane Fonda woman elbowed me out for the #4 spot!

[caption id="attachment_4452" align="alignright" width="574" caption="Wheat Belly hits #5 on New York Times Bestseller List--in 1st week!"][/caption]

Interview with Jimmy Moore of Livin' La Vida Low-Carb

Here's my podcast interview with Jimmy Moore, host of the Livin' La Vida Low-Carb Show. (If you want to fast forward to the interview, go to time marker 41:20 on the slidebar.)



In the podcast, I talk about how the Track Your Plaque program and its focus on lipoprotein testing, along with the need to reverse the incredible epidemic of diabetes and pre-diabetes, led to elimination of all wheat from the diet and the book, Wheat Belly.

An open letter to the Grain Foods Foundation

Readers: Please feel free to reproduce and disseminate this letter any way you see fit.


To:

Ms. Ashley Reynolds
490 Bear Cub Drive
Ridgway, CO 81432
Phone: 617.226.9927
ashley.reynolds@mullen.com


Ms. Reynolds:

I am writing in response to the press release from the Grain Foods Foundation that describes your effort to "discredit" the assertions made in my book, Wheat Belly: Lose the wheat, lose the weight and find your path back to health. I'd like to address several of the criticisms of the book made in the release:

" . . . the author relies on anecdotal observations rather than scientific studies."
While I do indeed have a large anecdotal experience removing wheat in thousands of people, witnessing incredible and unprecedented weight loss and health benefits, I also draw from the experiences already documented in clinical studies. Several hundred of these studies are cited in the book (of the thousands available) and listed in the Reference section over 16 pages. These are studies that document the neurologic impairment unique to wheat, including cerebellar ataxia and dementia; heart disease via provocation of the small LDL pattern; visceral fat accumulation and all its attendant health consequences; the process of glycation via amylopectin A of wheat that leads to cataracts, diabetes, and arthritis; among others. There are, in fact, a wealth of studies documenting the adverse, often crippling, effects of wheat consumption in humans and I draw from these published studies.


"Wheat elimination 'means missing out on a wealth of essential nutrients.'"
This is true--if the calories of wheat are replaced with candy, soft drinks, and fast food. But if lost wheat calories are replaced by healthy foods like vegetables, nuts, healthy oils, meats, eggs, cheese, avocados, and olives, then there is no nutrient deficiency that develops with elimination of wheat. There is no deficiency of any vitamin, including thiamine, folate, B12, iron, and B6; no mineral, including selenium, magnesium, and zinc; no polyphenol, flavonoid, or antioxidant; no lack of fiber. With regards to fiber, please note that the original studies documenting the health benefits of high fiber intake were fibers from vegetables, fruits, and nuts, not wheat or grains.

People with celiac disease do indeed experience deficiencies of multiple vitamins and minerals after they eliminate all wheat and gluten from the diet. But this is not due to a diet lacking valuable nutrients, but from the incomplete healing of the gastrointestinal tract (such as the lining of the duodenum and proximal jejunum). In these people, the destructive effects of wheat are so overpowering that, unfortunately, some people never heal completely. These people do indeed require vitamin and mineral supplementation, as well as probiotics and pancreatic enzyme supplementation.


I pose several questions to you and your organization:

Why is the high-glycemic index of wheat products ignored?
Due to the unique properties of amylopectin A, two slices of whole wheat bread increase blood sugar higher than many candy bars. High blood glucose leads to the process of glycation that, in turn, causes arthritis (cartilage glycation), cataracts (lens protein glycation), diabetes (glycotoxicity of pancreatic beta cells), hepatic de novo lipogenesis that increases triglycerides and, thereby, increases expression of atherogenic (heart disease-causing) small LDL particles, leading to heart attacks. Repetitive high blood sugars that develop from a grain-rich diet are, in my view, very destructive and lead to weight gain (specifically visceral fat), insulin resistance, leptin resistance (leading to obesity), and many of the health struggles Americans now experience.

How do you account for the psychologic and neurologic effects of the wheat protein, gliadin?
Wheat gliadin has been associated with cerebellar ataxia, peripheral neuropathy, gluten encephalopathy (dementia), behavioral outbursts in children with ADHD and autism, and paranoid delusions and auditory hallucinations in people with schizophrenia, severe and incapacitating effects for people suffering from these conditions.

How do you explain the quadrupling of celiac disease over the last 50 years and its doubling over the last 20 years?
I submit to you that, while this is indeed my speculation, it is the changes in genetic code and, thereby, antigenic profile, of the high-yield semi-dwarf wheat cultivars now on the market that account for the marked increase in celiac potential nationwide. As you know, "hybridization" techniques, including chemical mutagenesis to induce selective mutations, leads to development of unique strains that are not subject to animal or human safety testing--they are just brought to market and sold.

Why does the wheat industry continue to call chemical mutagenesis, gamma irradiation, and x-ray irradiation "traditional breeding techniques" that you distinguish from genetic engineering? Chemical mutagenesis using the toxic mutagen, sodium azide, of course, is the method used to generate BASF's Clearfield herbicide-resistant wheat strain. These methods are being used on a wide scale to generate unique genetic strains that are, without question from the FDA or USDA, assumed to be safe for human consumption.

In short, my view on the situation is that the U.S. government, with its repeated advice to "eat more healthy whole grains," transmitted via vehicles like the USDA Food Pyramid and Food Plate, coupled with the extensive genetic transformations of the wheat plant introduced by agricultural geneticists, underlie an incredible deterioration in American health. I propose that you and your organization, as well as the wheat industry and its supporters, are at risk for legal liability on a scale not seen since the tobacco industry was brought to task to pay for the countless millions who died at their product's hands.

I would be happy and willing to talk to you personally. I would also welcome the opportunity to debate you or any of your experts in a public forum.

Wiliam Davis, MD
Author, Wheat Belly: Lose the wheat, lose the weight and find your path back to health (Rodale, 2011)
Does high cholesterol cause heart disease?

Does high cholesterol cause heart disease?

How often does someone develop coronary heart disease from high cholesterol alone?

Believe drug industry propaganda and you'd think that everyone does. Physicians have bought into this concept also, driving the $27 billion annual sales in statin cholesterol drugs.

In my experience, I can count the number of people who develop coronary disease from high cholesterol alone on one hand. It happens--but rarely.

That's not to say that cholesterol is not an issue. That rant populates many of the kook websites and conversations on the internet that argue that high cholesterol is a surrogate for some other health issue, or that it is part of a medical conspiracy.

The problem with conventional measurement of cholesterol is that it ignores the particle size issue: whether particles are large or small. Small LDL are flagrant causes of coronary atherosclerotic plaque. Large LDL is a rather meager cause. Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.

The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

It is therefore an unfortunate oversimplification to say that high cholesterol causes heart disease or that it doesn't. It can--but not always, depending on size and other factors. In my view, it is therefore irreponsible to treat total or LDL cholesterol without knowledge of particle size. I've seen this play out many times: Someone with an LDL cholesterol of 150 mg/dl but all large still gets prescribed a statin drug by his/her doctor. Or someone with an LDL of 100 mg/dl--generally "favorable" by most standards--is not treated but it is all small and the person is truly at high risk. (Also, knowledge that all LDL particles are small does not mean that statins are the preferred agent. In my view, they are not.)

Comments (15) -

  • Anonymous

    10/3/2008 4:41:00 AM |

    I've had no success lowering my very high LDL(350), can't tolerate statins..supposedly have combination of large and small LDL, 20-40% blockages per cardiac cath.My HDL (80), Trig.(70)are good, but still concerned since already show athrosclerosis. I'm 55, 100 lbs., and have had high LDL since a teen. Any suggestions? Thanks!

  • Anonymous

    10/3/2008 5:25:00 PM |

    Isn't inflammation the root cause of atherosclerosis ? Isn't cholesterol's role in heart disease only that it happens to be used as the material, with which the body repairs the lesions caused by inflammation ?

  • Steve

    10/3/2008 6:16:00 PM |

    excellent post. 1. if statins not preferred way to go for small LDL, what is- Niacin and elimination of grains? 2. How is it possible that a VAP test showed large Pattern A(by small margin)and two years later NMR shows nearly 100% small dense Pattern B?  Is one test better than the other? 3. Do genetics overwhelmingly determine pattern size?  I have eliminated all grains,sugars, starchy veggies to see if i can get my LDL to be large and fluffy.  Thank you.

  • Anne

    10/4/2008 5:17:00 PM |

    I am an example of someone with "normal" cholesterol and CAD. I was only 54 years old when my LAD blocked. I went on to bypass as I reblocked after each stent.

    In the past few years I have been looking into many of the other factors may have contributed to my  health problems and trying to optimize my health. Yes, coromary heart disease is so much more than elevated cholesterol.

  • Stan (Heretic)

    10/4/2008 5:37:00 PM |

    No it doesn't!

  • Peter

    10/5/2008 2:41:00 PM |

    Hi Dr Davis,

    Excellent post. The value of total cholesterol is irrelevant. While there is a VERY slightly higher cholesterol level in heart attack patients, the overlap with the normal population is such as to make total cholesterol level meaningless. Once it's meaningless and you can then look back to the initial work of Ancel Keys, who appears to have been the primary architect of the lipid hypothesis, and you can see it is based on this now clearly meaningless measurement.

    The very slight increase in TC in cardiac patients is explicable by the fact that glycation of the apoA particle inhibits its attachment to the LDL receptor. I would expect this to produce a slight rise in TC. You then have to pose the question as to which does most damage: persisting apoA containing particles due to glycation of their surface protein, or glycation of all of the body proteins by the same hyperglycaemia that affected the apo A protein. Using HbA1c as a marker of hyperglycaemia there is a reasonable correlation with CVD even within "normal" HbA1c levels in the EPIC study. Whole grains = hyperglycaemia. Hyperglycaemia = apoptosis of vascular endothelium. What more do you need for vascular damage?

    So, as the lipid hypothesis is based on TC and should have been stillborn or drowned at birth, where does particle size come in? We have the situation of good (HDL) cholesterol and bad (LDL) cholesterol to explain why TC is useless. Then we get good LDL (large fluffy) and bad LDL (small dense) to explain why total LDL (by calculation) is utterly useless too. We even now have good and bad HDL. Never mind good (small) VLDL and bad (large) VLDL to explain why some triglycerides are better/worse than others.

    Ultimately small dense LDL, large VLDL and HDL3 are strong markers of the metabolic syndrome. Hyperinsulinaemia and insulin resistance are the cornerstones of metabolic syndrome according to Reaven, who largely popularised the concept. The lipid changes are easily viewed as a consequence, not a cause, of metabolic syndrome. It is undoubtedly believable that sdLDL is stickier/more oxidisable than other lipoproteins, but that becomes unimportant if it's not there in the first place, ie no metabolic syndrome. This would, simply, explain why reducing wheat products works to reduce sdLDL, unless they are replaced by equally insulinogenic "wheat free" comparable junk foods based on non wheat sugar sources. If it turned out that purple spotted LDL, induced by eating blackberries, was stickier than sdLDL we would no doubt have a drive to eliminate blackberries or (more likely) develop a drug to remove the purple spots.

    Following your blog gives me the distinct impression that one day you really could become a cholesterol skeptic. Stranger things have happened.

    Peter

  • JayCee Botha

    10/6/2008 9:37:00 PM |

    Anonymous and Steve - I stronly believe in a propper low carb (note that I say LOW carb, and not NO Carb) way of eating. I would really like to suggest some awesome reading material. It is from dr. James E Carslon who wrote the book "Genocide. How your doctors dietary ignorance will kill you!!!". In the book he explains amongst other things the actual benefits of dietary cholesterol and how a low-carb way of eating will increase the ldl-particle sizes and bring down the triglycerides and dangerous VLDL.

    From a recent personal answer I got from him, he explained to me the benefits of adding dietary cholesterol from a biochemical point of view. I hope this helps in understanding that a correct dietary change can help.

    Here is what he said :

    OK, so what are the benefits of adding cholesterol to the diet? It's not only fascinating, it'll blow your mind. When we eat cholesterol containing foods, the cholesterol in the food we consume actually binds to an enzyme called HMG CoA reductase and inhibits its function. This enzyme is what's known as the rate limiting enzyme in cholesterol biosynthesis. This means that once this enzyme does what it's supposed to do, cholesterol will be made no matter what. By inhibiting the enzyme's function, choilesterol cannot be made. So eating cholesterol actually inhibts its own production.
    But wait, it gets even better.

    The cholesterol in the foods we eat is what's referred to as fat soluble, or lipophilic (or fat loving). Since cholesterol is lipophilic, it diffuses through not only the outer cell membrane, but the cell's=2 0nucleus membrane and attaches the the DNA. Guess where it attaches to on the DNA? It attaches to the sites on DNA WHERE HMG Co A IS MADE!!!!! That's right, so not only does the cholesterol in the food we eat attache and inhibit the function of the enzyme already present to make cholesterol; the cholesterol in the foods we eat also prevents the production of the enzymes needed to make itself. In biochemical speak, this is known as negative biofeedback.

    Eat more cholesterol, make less cholesterol. By the way, the only thing I've seen in eighteen years considerably raise the good cholesterol known as the HDL, is the consumption of more cholesterol. So EAT MORE CHOLESTEROL IT"S GOOD FOR YOU!

  • moblogs

    10/7/2008 12:11:00 PM |

    Inflammation is essentially the cause of heart disease isn't it?
    I'm not medically trained, but I assume small particle LDL is a signifier of crammed, broken up large particles - perhaps a long time accumulation of what was once sent to the skin hoping to be converted to D by UVB but didn't(there is a study that says British gardeners have lower cholesterol in the Summer which seems very interesting).
    The fact that statins work (albeit with alarming side effects), and that according to a Spanish study, that atorvastatin raises vitamin D some degree shows the problem isn't really cholesterol. That is erroneous cholesterol readings are the 'symptom' of either vitamin D deficiency or associated things that domino on to the ability for the heart to succomb to heart disease. As a rule I still think the general cholesterol hypothesis is a farce, not just because of the way the products are marketed but because it's only looking at one station on the tube system. 'High cholesterol causing heart disease' might be better termed as 'low vitamin D causes heart disease' because that's perhaps the root, or at least one root.

  • Steve L.

    11/14/2008 5:43:00 AM |

    Dr. Davis,

    First let me say a big thank you for your blog.  I follow your's, Jimmy Moore's and the Drs. Eades' blogs closely.  As a result of reading your book and blot, I just had my first heart scan at age 50, and was vert happy to hear zero calcium score.

    I do low carb nutrition (~50g/day), so my triglycerides were very low (28).  I've read that all LDL will be large with triglycerides that low (below 70).  Can you confirm that?  Would I be wasting my money on blood work to determine particle size?  HDL is 62, LDL 136.

    Steve L.

  • Wenchypoo

    4/9/2009 1:14:00 PM |

    Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

    Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.


    I'm looking for heart disease info that isn't related to cholesterol OR grain intake, because my cat has it--cats are obligate carnivores, and therefore do not take in grains unless fed commercially-prepared foods.  Mine do not--I make their food from scratch, using a UC Davis vet-designed diet recipe.  Cholesterol levels aren't a concern either, although I now know to have the SIZE of cells examined, as well as vitamin D levels checked.  As for anti-inflammatories, fish oil is part of the diet recipe.

    I'm going back to the vet for more blood work (now that I have more clues).

  • TedHutchinson

    10/1/2010 8:48:09 AM |

    Statins Do Not Decrease Small, Dense Low-Density Lipoprotein
    Free full text at link.
    In an observational study, we examined the effect of statins on low-density-lipoprotein (LDL) subfractions.
    Using density-gradient ultracentrifugation, we measured small, dense LDL density in 612 patients (mean age, 61.7 ± 12.6 yr), some with and some without coronary artery disease, who were placed in a statin-treated group (n=172) or a control group (n=440) and subdivided on the basis of coronary artery disease status.
    Total cholesterol, LDL cholesterol, apolipoprotein B, and the LDL cholesterol/apolipoprotein B ratio were significantly lower in the statin group. However, the proportion of small, dense LDL was higher in the statin group (42.9% ± 9.5% vs 41.3% ± 8.5%; P=0.046) and the proportion of large, buoyant LDL was lower (23.6% ± 7.5% vs 25.4% ± 7.9%; P=0.011). In the statin group, persons without coronary artery disease had higher proportions of small, dense LDL, and persons with coronary artery disease tended to have higher proportions of small, dense LDL.
    Our study suggests that statin therapy—whether or not recipients have coronary artery disease—does not decrease the proportion of small, dense LDL among total LDL particles, but in fact increases it, while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL. If and when our observation proves to be reproducible in subsequent large-scale studies, it should provide new insights into small, dense LDL and its actual role in atherogenesis or the progression of atherosclerosis.

  • buy jeans

    11/3/2010 6:19:10 PM |

    The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

  • Mary

    1/25/2011 8:42:22 PM |

    For years I suffered from high cholesterol and was almost permanently on statin medication. I come for a family with a strong history of heart disease and I personally believe that high cholesterol can cause heart disease. Thankfully I now have my cholesterol under control but it has been hard work, and I done it the natural way, as I suffered from the side effects statins cause.

    How To Lower Cholesterol Without Medication

  • Anonymous

    3/12/2011 8:55:30 AM |

    About eighty percent of our cholesterol is produced by the liver and the rest depends on our diet. Foods such as red meat and butter are rich in cholesterol where as those from plant origin have very little or no cholesterol at all. The control of cholesterol in our body is done by the liver. I think,more can be found out from:
    http://www.heart-consult.com/articles/how-cholesterol-affects-heart

  • doug

    5/9/2011 8:52:46 PM |

    exactly!!!!!

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