Diabetes: Better than hedge funds

Diabetes is where the action is.

While, for virtually all of history, type 2 diabetes was an uncommon condition of adults, the disease has spread so much to all levels of American society that even kids are now developing the adult form. Researchers from the Center for Disease Control and Prevention predict that, by 2050, one in three adults will be diabetic.

The diabetes market is booming, handily surpassing growth of the oil industry, the housing market, even technology. It makes Bernie Madoff’s billions look like small potatoes. In health, few markets are growing as fast as diabetes—-not osteoporosis, not heart disease, not cancer.

Americans are getting fat from carbohydrate consumption, becoming diabetic along with it. While kids hanging around the convenience store gulp down 26 teaspoons of sugar in 32-ounce sodas and 56-grams-of-sugar in 16-ounce frozen ices, health-minded adults are more likely eating two slices of 6-teaspoons sugar-equivalent “healthy whole grain” bread, wondering why last year’s jeans are too tight.

The U.S. is not the only nation affected. Globally, 2.8% of the world’s population are diabetic, a number expected to double over the next 20 years.

Pharmaceutical companies boast double-digit growth for diabetes drugs, growth rates that keep profit-hungry investors happy. Merck’s Januvia, for instance, introduced in 2006, recently catalogued 30% growth in sales, with annual sales approaching $1 billion. Recently FDA-approved Victoza, requiring once-a-day injection, is expected to reap $4 billion in sales per year for manufacturer Novo Nordisk. Such numbers can only warm a drug company CEO’s heart.

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon.

“Collateral” revenues from the other health conditions that develop from a diet rich in “healthy whole grains,” such as drugs for hypertension, drugs to slow the progression of kidney disease in diabetes, drugs for “high cholesterol,” and drugs for high triglycerides, and you have a pharmaceutical drug bonanza. You, too, would throw all-expenses-paid, fly-the-entire-sales-force-to-the-Caribbean sales meetings.

The global diabetes market has already topped $25 billion and is growing at double-digit rates. Forget the Internet, gold stocks, or solar energy—-diabetes is where the money is. This fact has not been lost on the very market-savvy pharmaceutical industry. As with any successful business, they have devoted substantial resources to develop and grow this booming business.

270 lb man in diapers

Alex is a big guy: 6 ft 4 inches, 273 lbs.

On 10,000 units per day of vitamin D in gelcap form, his 25-hydroxy vitamin D level was 38.4 ng/ml. One year earlier, his 25-hydroxy vitamin D level, prior to any vitamin D supplementation was 9.8 ng/ml.

According to the latest assessment offered by the Institute of Medicine (IOM):

Vitamin D need for a 13-month old infant: 600 units per day

Vitamin D need for a 6 ft 4 in, 273 lb male: 600 units per day

I paint this picture to highlight some of the absurdity built into the smug assumptions of the IOM's report. It would be like trying to fit a large, full-grown man into the diapers of a 13-month old. Few nutrients or hormones (in fact, I can't think of a single one) are required in similar quantity by an infant or toddler and a full grown adult. However, according to the IOM's logic, their vitamin D needs are identical, regardless of age, body size, skin color, genetics, etc. One size fits all.

Just as the original RDA assessment by the Institute of Medicine kept thinking about vitamin D somewhere in the Stone Age, so does this most recent assessment.

90% small LDL: Good news, bad news

Chris has 90% small LDL particles.

On his (NMR) lipoprotein panel, of the total 2432 nmol/L LDL particles ("LDL particle number"), 2157 nmol/L are small, approximately 90% (2157/2432).

Bad news: Having this severe excess of small LDL particles virtually guarantees heart attack and stroke in Chris' future.

Good news: It means that Chris potentially has spectacular control over his lipoprotein and lipid values, achieving statin-like values without statin drugs.

Typically, extravagant quantities of small LDL particles are accompanied by low HDL, high triglycerides, and pre-diabetes or diabetes. Chris' HDL is 26 mg/dl, triglycerides 204 mg/dl; HbA1c 5.9% (a reflection of prior 60-90 days average blood glucose; desirable 4.8% or less), fitting neatly into the expected pattern.

Chris' pattern tells me several things:

1) He overconsumes carbohydrates, since carbohydrates trigger this pattern.
2) He likely has a genetic susceptibility to this effect (e.g., a variant of the gene for cholesteryl ester transfer protein, perhaps hepatic lipase). Only the most gluttonous and overweight carbohydrate consumers can generate this high a percentage small LDL without an underlying genetic susceptibility.
3) Provided he follows the diet advised, i.e., elimination of all wheat, cornstarch, oats, and sugars, he is likely to have an extavagant drop in LDL particle number. Should he achieve the goal I set of small LDL of 300 nmol/L or less, his LDL particle number will likely be around 500 nmol/L. This translates to an LDL cholesterol of 50 mg/dl . . . 50 mg/dl.

In many people, this notion of taking statin drugs for "high cholesterol" is an absurd oversimplification. But it is a situation that, for many, is wonderfully controllable with the right diet.

The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.
Why haven't you heard about lipoprotein(a)?

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

Comments (26) -

  • Matt Stone

    7/1/2010 4:18:14 PM |

    Ah, thyroid normalization. My favorite. Of course, this has a trickle-down effect on DHEA, estrogen, and testosterone as well. Perhaps Lp(a) is one mechanism by which Broda Barnes was able to prevent heart attacks in his patients?  

    http://180degreehealth.com

  • Anonymous

    7/1/2010 4:39:21 PM |

    Aw darn it. Again health info to be confused about. From Taubes' GCBC I read it was apoB supposed to be the one associated with smaller and denser LDL, "the bad LDL", and I thought apoA was the "large and fluffy" or more benign LDL. I'm pretty sure Dr. Lustig says pretty much the same in his "Sugar, the bitter truth" video. There goes my newly acquired "understanding" out the window again.

  • Anonymous

    7/1/2010 4:42:40 PM |

    The last of the 4 treatments doesnt' seem very specific...

    is "T3" a supplement.. if not, how does one go about normalizing the Thyroid?

  • Mike

    7/1/2010 8:12:19 PM |

    That's a lot of fish oil. I take about 1/5 that amount and would find it irritating to have to increase my intake by a factor of 5.

  • Drs. Cynthia and David

    7/1/2010 9:52:19 PM |

    If the pharma industry could actually come up with drugs that work and don't just chase surrogate markers, I'm sure that would be helpful.  I'm all for nutritional and lifestyle fixes, but this won't work perfectly for everyone all the time, so useful drug therapies would be nice too.

    Anonymous, I think you're confusing LDL pattern A and B ("fluffy" vs dense) with apoA and ApoB (HDL associated vs LDL associated proteins).

    Cynthia

  • Anthony

    7/1/2010 10:20:10 PM |

    Dr. Davis,
    How low do you like to see Lp(a)? I've seen recommendations of below 30mg/dl, below 20, and below 10. Mine is 19. Thanks,

    Anthony

  • Dr. William Davis

    7/2/2010 1:12:23 AM |

    Anthony-

    Excellent question . . . for which there's no solid answer.

    Despite all we know about Lp(a), no endpoint data have been generated. However, I can tell you that using particle count measurements in nmol/L a level of 60 nmol/L works very well. In mg/dl, a measure of weight per volume, it depends on the method of measurement used. If the "normal" range is 30 mg/dl or less, then aiming for around 20 mg/dl has worked well.

  • Anonymous

    7/2/2010 1:32:33 AM |

    I asked my cardiologist about it (heads up preventive cardiology at a major research institution in Texas) and he said:

    "Well, there's not anything we can do about it, so why test it?"

  • Anonymous

    7/2/2010 1:55:40 AM |

    My cardiologist and PCP have never ever discussed this with me even though I brought it up for discussion. I think my PCP didn't know much and ignored it. I desperately need a new cardiologist (I live in the SF bay area). Anybody here love their cardiologist and like to share some details? I will be forever thankful Smile

    TIA

  • Paul

    7/2/2010 6:09:32 AM |

    I found this to be a very interesting post over at the Animal Pharm blog concerning this very subject:
    Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat


    They basically come to a very simple conclusion in controlling Lp(a); eat some damn saturated fat! And stay away from the damn carbs!

    Now, let me get back to making my LDL the plain and fluffy kind... someone pass me the ghee please...

  • Harry

    7/2/2010 2:41:24 PM |

    Anonymous and Drs. Cynthia and David, there are several "A" designated particles that frequently get confused. Dr. Davis is talking about lipoprotein(a), with a lower case "a", which consists of an LDL particle with a particle of apolipoprotein(a) attached to it. This apolipoprotein is also designated by a lower case "a". Lp(a) is very atherogenic, and should be minimized.

    Apolipoprotein A, with an upper case "A", on the other hand, is an atheroprotective particle that is a component of HDL. It comes in several varieties. The most plentiful one is designated Apolipoprotein A-I, or Apo A-I, which is the main particle that participates in reverse cholesterol transport, which is the principal way that HDL protects against atherosclerosis, by removing cholesterol from plaque and transporting it back to the liver for disposal. There are also particles designated Apo A-II and Apo A-IV that are also associated with HDL, but their function is not well understood. All the HDL-associated apo A particles are described with the upper case "A".

    Finally, there is the LDL pattern A, which indicates that the LDL particles are mostly large, whereas LDL pattern B indicates that LDL particles are mostly small. These are usually designated with an upper case "A" and "B", and the A pattern is thought to be less atherogenic than the B pattern.

    It is easy to confuse these "A" types, especially Apo A and Apo a, which are two very different particles, the large A apo is good and the small a apo is bad.

  • Kent

    7/2/2010 3:21:25 PM |

    My LP(a) started a year and a half ago at 198 nmol/L, it is now down to 35 nmol/L. Thanks to Dr, Davis's advice that I followed in the Track Your Plaque book, including 4800mg combined EPA, DHA fish oil and 2000mg Niaspan, etc.

    I also want ot mention though that I have been following the Linus Pauling protocol as well, which I believe has a synergistic effect with the other principles applied.

    An interesting thing happened that is worth mentioning, my LP(a) had been gradually dropping over that period of a year and a half from 198 to 45 nmol/L, then I switched to immediate release niacin and my LP(a) jumped back up to 150 nmol/L. That was the only change I made, so I switched back to Niaspan and that is when it went back down to 35 nmol/L.

    Kent

  • Alfredo E.

    7/2/2010 3:35:40 PM |

    Hi All.The following paragraphs were taken from http://www.drlam.com/opinion/Lp(a).asp

    Lipoprotein A, commonly called Lp(a), is a major independent risk factor for cardiovascular disease. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl.

    Currently, there is no medicine or drugs that to effectively lower your Lp(a). A high Lp(a) is genetically linked. Fortunately, Mother Nature has provided us a much better non-toxic alternative. It consists of large doses of vitamin C, L-lysine, and L-proline.

    Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.

    This last flower:
    Replacing carbohydrates with proteins ignores the fact that protein, once in the intestinal tract, converts to amino acid. Amino acids increase insulin secretion. It is unclear, however, whether proteins are as potent as carbohydrates in stimulating insulin secretion.

    My comment: Is it possible that protein can produce high insulin secretion? So, what is left for simple humans? No carbs, no protein?

  • Anonymous

    7/2/2010 3:52:13 PM |

    Is the LDL carried in the blood by a protein or has it already been oxidized. I'm trying to understand what form chlorestral is in the blood.

  • David

    7/2/2010 6:17:02 PM |

    Alfredo,

    It's true that protein stimulates insulin, but the key is that it doesn't only stimulate insulin. Glucagon, insulin's counter-regulatory hormone, is also stimulated. Insulin secretion  is undesirable in the context of low glucagon (which is what we have with high carbohydrate intake), but it's not such a big deal when the ratio of the two are more balanced (which is what we have with low-carb protein intake).

    David

  • Jack C

    7/3/2010 12:03:08 AM |

    The VAP cholesterol profile, which gives the distribution of LDL and HDL particle sizes a other information, shows an upper limit of 10 mg/dl for Lp(a)cholesterol.

    In recent tests, my wife had an Lp(a) of 6 while mine was 8. Through no fault of our own I might ad.

  • Dr. William Davis

    7/3/2010 12:13:49 AM |

    HI, Kent--

    Great results!

    You are living proof that Lp(a) can indeed be tamed. It sometimes requires some unusual strategies, but huge reductions are possible . . . and Lipitor is not part of the equation.

    Long-term commitment to the effort is the key.

  • Anonymous

    7/3/2010 1:29:29 AM |

    what kind of doctor shoudl i see to get the right tests done.  I know I have high Lipo(a) from a previous test at Mayo.  They recommended that I take drugs and I declined.  Now I'm realizing I don't have the complete story.  I need to know more than just my lipo(a) is high.

    thanks!
    Linda

  • Anonymous

    7/3/2010 6:04:15 AM |

    Hi
    Are there stats on people with lp(a) that don't develop any plaque?
    Also does the same happen with lp(a) as with ldl? that is that is better to have a higher mg/dl with big paricles than a lower mg/dl with small particles?
    Santiago

  • Hans Keer

    7/3/2010 7:28:36 AM |

    I would say apoprotein(a) is normal phenomenon. What is not normal is the abundance of small dense LDL which apoprotein(a) binds to. So the best way to avoid LP(a), is to avoid the abundance of sugars and starch in the diet. All the other (still costing) treatments for Lp(a) won't be necessary then.

  • jd

    7/3/2010 5:39:38 PM |

    Hi,   I recently had a VAP test done via LEF -- I seem to have some very good numbers and some bad LDL ones.  Any comments would be appreciated.

    all values in mg/dl
    LDL 105
    HDL 71
    VLDL 14
    Total Cholesterol 190
    Triglycerides 51
    LP(a) 4.0
    IDL 3
    HDL2 18
    HDL3  53
    VLDL3 8
    LDL1 PatternA 5.4
    LDL2 PatterA 7.5
    LDL3 PatternB 61.6
    LDL4 PatternB 22.4


    LDL Density pattern = B, flagged abnormal

    Vit D  65.4 ng/ml
    Homocysteine 6.2
    C-Reactive Protein 0.2

    I am 55 yr of age, 6'0", 165 lbs, exercise regularly.

    Heart disease in family, mother's father died of heart attack at 66, other 3 grandparents lived into 90s.  father died leukemia cancer 53, mother living at 80 in good health.  Thanks,   Jim

  • Anonymous

    7/7/2010 4:40:46 PM |

    I use Lugols solution 2% and I have absolutely no idea what dosage I should be using.  I have been using one drop about twice a week, but I would like to have a better idea of proper dosage.  Can you help?

  • James L.

    7/13/2010 9:52:15 PM |

    My cardiologist is treating my high Lp(a) with Niaspan, but even with high doses, it has not had much effect. What do you mean by items 3 and 4 on DHEA and T3? Please be more specific. Thanks.

  • Anonymous

    7/29/2010 9:06:55 PM |

    Could you give some dose for T3 and DHEA that you are recommending?

    Thanks!

  • Anonymous

    8/10/2010 8:38:43 AM |

    "If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. "

    Does that mean that high levels of Lp(a) is not inherited from the father?

    Thanks

  • LisaMichelle

    8/24/2011 11:46:03 PM |

    Dear Dr. Davis,

    I'm a 44 yr old female.   I recently had a consultation w/ a cardiologist here in Canada.   I was sent for the consultation because of some strange left jaw and low chest tightness I'd experienced at work the week prior (had been seen then in the ER, normal ECG x 2, normal CXR, normal bloodwork).  Prior to the appt I was told I needed to have fasting bloodwork (so that results were available for the cardiologist to review at my appt).  

    HDL good, LDL good (though at the higher end of the normal range).  Lipoprotein A was 0.55 g/L (which i guess works out to 55 mg/dl which is what the usual unit of measurement is for this one in the U.S.).  The cardiologist told me that all of my bloodwork was normal and that I was very low risk for a heart attack but I requested a copy of my results just to have on file.   I am surprised she didn't mention the elevated Lipoprotein A (normal range for this lab is: 0.00 to 0.33 g/L).   So that got my on my search for info on what exactly Lipoprotein A is, and what it indicates.

    My question is:   I was only told to fast for 12 hours prior to my bloodwork, nothing was said about ensuring I didn't smoke.   Well I did smoke over the 12 hours up until the blood was drawn (even about 30 minutes prior to).   Now I'm reading online that one should not smoke prior to blood being drawn for Lipoprotein A, HDL and LDL, etc.    So could my smoking right up to the time bloodwork done have negatively impacted the results?   Could smoking have made my LDL and Lipoprotein A higher?    Should I have these redone but ensure I don't smoke for 12 hrs prior to blood draw?  (I have a 'quit date' set for next Saturday, so don't worry, I will be quitting).

    Thanks so much,
    Lisa

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Green tea: friend or faux?

Green tea: friend or faux?

The www.HealthCastle.com website is a helpful website on healthy eating that sends out a free newsletter. The content is all produced by licensed dietitions and nutritionists. Although I don't agree with everything said on the site, there's still some good information.

I'm a fan of green tea. Although I believe the effects are relatively modest (weight reduction, cholesterol reduction, anti-oxidation, etc., with theaflavin and/or green tea as a beverage,) they alerted me to the fact that the Lipton Green Tea product is one you should steer clear of. Here are their comments:



"More like Soft drink than Green Tea!With 200 calories, 13 teaspoons of added sugar and a long list of artificial ingredients, Lipton Iced Green Tea is more like a bottle of soft drink than tea, in our opinion."


The Lipton website lists the ingredients:

Water, high fructose corn syrup, citric acid, green tea, sodium hexametaphosphate, ascorbic acid (to protect flavor), honey, natural flavors, phosphoric acid, sodium benzoate (preserves freshness), potassium sorbate (preserves freshness), calcium disodium edta (to protect flavor), caramel color, tallow 5, blue1.

An 8 oz serving yields 21 grams of sugar. If you drink the full 20 oz. bottle (not hard to do!), that yields 52.5 grams of sugar! You will also notice that the second ingredient listed after water is high fructose corn syrup. This ingredient, you may recall, causes triglycerides to skyrocket, causes an insatiable sweet tooth, and is a probable contributor to obesity and diabetes.

In their defense, the Lipton people do also offer a sugar-free alternative without the excessive sweeteners and empty calories.

Do the Lipton products offer the same kind of benefits from green tea catechins (flavonoids) offered by freshly brewed teas? This product has not been formally tested by an independent lab to my knowledge, though, in general, commercially prepared and bottled teas tend to have dramatically less catechin/flavonoid content compared to brewed. (The USDA website provides access to an extraordinary collection of flavonoid food content at their USDA Database for the Flavonoid Content of Selected Foods - 2003. You'll find it at http://www.ars.usda.gov/Services/docs.htm?docid=6231.)

I think the HealthCastle people got it right: Brew your own, making sure to steep for at least 3 minutes. Alternatively, a green tea or theaflavin supplement provides many of the benefits. (Theaflavin has been used in trials at doses of 375 to 900 mg per day.) An in-depth report on green tea will be coming in a future Special Report on the www.cureality.com Membership website.
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Fish oil for $780 per bottle

Fish oil for $780 per bottle

At prevailing pharmacy prices, one capsule of prescription Lovaza fish oil costs $4.33 each.

Yes, you heard right: $4.33 per capsule.

What do you get for $4.33 per capsule? By omega-3 fatty acid content, you get 842 mg EPA + DHA per capsule.

I can also go to Sam's Club and buy a bottle of their Triple-Strength fish oil with 900 mg omega-3 fatty acids per capsule at $18.99 per bottle of 180 capsules. That comes to 10.5 cents per capsule. That puts the price of fish oil from Sam's Club at 97.6% less cost compared to Lovaza for an equivalent quantity of omega-3 fatty acids.

What if we repriced Sam's Club's Triple-Strength and brought it "in line" with what we pay for Lovaza? That would put the value of one bottle of Sam's Club Triple-Strength fish oil at $780 per bottle.

I take patients off Lovaza every chance I get.

Comments (16) -

  • Cathy

    8/19/2009 10:31:05 PM |

    Thanks for that.  I still take Lovaza; have been lazy about switching.  I just checked the price my mail-order pharmacy pays and it's $546 per bottle of 120, or just over $1.50 per capsule.  While considerably less than what you quoted, it's still $6 per day and $2185 per year!  I'd no idea.  Plus I take Niaspan for another $900 per year.  I'm switching to OTC for both.  No wonder insurance rates are going up!

  • John Smith

    8/19/2009 11:16:18 PM |

    It's amazing how much some of these companies will try to scam people with 'pharmacy grade' vitamins. It's easy for me to tell how much fish oil is oxidized by taste and how well it works and the best brand I've found is from trader joe's for 8 bucks a bottle. For stuff like vitamin C the process is so simple it's pretty much literally impossible to have any real difference brand to brand aside from how absorbable it is and again it's easy to tell when pills are not absorbing due to how they feel.

  • Clamence

    8/20/2009 12:26:19 AM |

    And we wonder why healthcare costs are spiraling out of control in america...

    What's sad, is the problem isn't limited to just pharmaceuticals, so many other areas like diagnostic imaging and durable medical goods are so much more expensive than they should be.

  • Dr. William Davis

    8/20/2009 1:40:55 AM |

    Do your part to reduce healthcare costs: Reject the idea that fish oil, niacin, and vitamin D should be costly prescription agents.

    Pay for them yourself for SUPERIOR preparations that you can obtain without a prescription. This small effort alone will save us all hundreds of millions of dollars.

  • Nameless

    8/20/2009 3:04:42 AM |

    Anyone know when Lovaza is going generic? I thought I read that perhaps by end of the year their exclusivity may be up, which should open up cheap prescription alternatives -- and sort of kill Lovaza's profits too.

  • Anonymous

    8/20/2009 3:09:24 AM |

    I use otc niacin at about $3 a bottle, and one of the doctors I work with asked me why I hadn't asked my doc for a prescription for Niaspan.
    I just didnt know where to begin.

    Jeanne

  • Anne

    8/20/2009 7:54:19 AM |

    Wow - I'm so surprised that there are worries about a national health care service in the US such as we have in the UK. Here, Lovaza (Omacor) costs the National Health Service £50 for 100 capsules, ie 50p per capsule !

    Of course that's not what patients pay. Patients who are charged prescription charges will pay  Â£7.20 per prescription of 100 capsules, and patients who don't pay prescriptions charges at all (approx 70% of patients), well they don't pay anything for their Lovaza....they have paid in their taxes for it already.

    But to me the biggest surprise is that the pharmacutical company that makes Lovaza charges so much less in the UK than it does in the US !

    Anne

  • Richard A.

    8/20/2009 6:32:00 PM |

    Another way to save on prescription drugs--pill splitting. Too often the smaller dose costs almost as much as the bigger dose. Getting the bigger pill and cutting it down to smaller doses can save a lot of money.

  • pyker

    8/20/2009 9:09:30 PM |

    I'm surprised we don't see scrips for "pharmaceutical-grade water", to wash these down.

  • Anonymous

    8/21/2009 2:21:12 AM |

    pyker, its called "bottled water"

  • JLL

    8/25/2009 1:38:15 PM |

    It's not really a problem that pharmacy grade fish oil is ridiculously expensive, as long as it's not illegal to sell cheaper fish oils too.

    In Europe, the trend seems to be that supplements are becoming available only in pharmacies, which can then charge extraordinary prices for everything.

  • Boris

    9/7/2009 1:22:32 PM |

    I have moderately high triglycerides at 255. My physician gave me a sample bottle of Lovazza to try which has 28 softgels. I have been taking one softgel a day.

    I have been looking into OTC fish oil supplements. Some are very diluted and some are very concentrated. Most break down the EPA and DHA content while others don't. I created a spreadsheet that collects the EPA and DHA content of several OTC fish oil supplement. In order to make a fair comparison, I adjusted my serving size for each brand name to give me about the same quantity of the essential fatty acids. The prices range from $0.11 per dosage to $1.76 per dosage.

    So once I figured out what's the most cost effective brand to buy now I have to worry and wonder about purity. Am I getting a less refined formula that will have heavy metals, PCBs, and other nasty chemicals? The words "triple distilled" mean nothing to me. I'd like to see "Contains no more than 0.010 PPM of arsenic" or something like that.

    The Lovazza might have the advantage here since the FDA probably won't let poisoned fish oil out. I have no idea what my effective price per dosage is with Lovazza since my sample bottle was free. My company takes a decent chunk of my pay for health care and I rarely use it. Maybe it's time I get my money's worth and get some subsidized Lovazza?

  • trinkwasser

    9/10/2009 2:51:21 PM |

    "I'm surprised we don't see scrips for "pharmaceutical-grade water", to wash these down."

    What, like this?

    http://www.marksdailyapple.com/bling-water/

  • Boris

    9/30/2009 4:29:47 PM |

    My one month experiment with Lovaza is over. I received a free sample bottle with 28 capsules last month from my physician. The recommended dosage was four a day but he told me to take one. I did that for one month. My triglycerides went down from 255 to 135 with no significant change in diet. My total cholesterol went down from 221 to 177, and it was all LDL. Unfortunately, my HDL levels stayed almost the same.

    So do I continue with Lovaza and get a prescription or do I get a high quality OTC like Omapure?

    I will see my physician tomorrow.

    Decisions, decisions, decisions!

  • moblogs

    3/24/2010 12:59:07 AM |

    Just want to add that Omacor (European Lovaza) costs £2 per day, while Triple Strength Omega 3 from a reputable company costs 12p per day in comparison, for roughly the same amount of EPA and DHA. You just have to take 6 capsules instead of 4.
    My jaw would've dropped if I hadn't been getting my vitamin D! Smile

  • buy jeans

    11/3/2010 9:50:53 PM |

    I can also go to Sam's Club and buy a bottle of their Triple-Strength fish oil with 900 mg omega-3 fatty acids per capsule at $18.99 per bottle of 180 capsules. That comes to 10.5 cents per capsule. That puts the price of fish oil from Sam's Club at 97.6% less cost compared to Lovaza for an equivalent quantity of omega-3 fatty acids.

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