Wheat brain

Among the most common effects of wheat are those on the brain.

Consume wheat and susceptible individuals will experience a subtle euphoria. Others experience mental cloudiness or sleepiness. (This is what I personally get.)

It gets worse. Children with ADHD and autism have difficulty concentrating on a task and have behavioral outbursts after a cookie. Schizophrenics experience paranoid delusions, auditory hallucinations, and worsening of social detachment. People with bipolar disorder can have the manic phase triggered by a breadcrumb. All these effects are blocked by administering drugs that block the brain's opiate receptors. (This is why, by the way, a drug company is planning to release an oral agent, naltrexone, formerly administered to heroin addicts to help control addiction, for weight loss: block the euphoric effect, take away the temptation, lose weight.)

Here is Heart Scan Blog reader, Nicole's, mental fog story:

I have been grain-free (no gluten free grains either) for quite a long time (about a year and a half). Earlier this week, I decided to try white bread and pasta. The experiment only lasted two days. I had horrible terminal insomnia both nights, causing me on the second night to wake up at 2:30 am unable to get back to sleep at all. I felt drugged and in a mind-fog all the next day and even dozed off a few times! Luckily I had the day off work.

I had very bad forgetfulness also. I forgot that I left my bag and groceries at work, so I had to go back for them. Then I had to use my husband's keys to get in because I thought my keys were in my bag, but it turns out they were in my pocket. Then I got my bag, set the alarm, locked the door and then realized I forgot my groceries. So I had to re-open the door, unset the alarm, and go back for the groceries. Then I locked the door, forgetting to set the alarm, so I had to unlock it, open up and set the alarm. It was just ridiculous, I am NEVER like that!

In addition to the insomnia and forgetfulness, I also had horrible anxiety and paranoia, almost to the point of panic. Which I NEVER have, I am usually very easy-going, even-tempered, and worry-free. But this was horrible, I really was quite paranoid and anxious about everything. Weird!

And the worst, was that in just two days of eating wheat, I gained 4 lbs and 2% bodyfat!! It's two days wheat-free now, and it's finally going back down, but wow. Just two days of wheat-eating caused that much weight and fat gain!

Anyway, I've learned my lesson and will continue to avoid grains (including gluten free grains) entirely.


Eat more "healthy whole grains"? Modern dwarf Triticum aestivum, perverted even further by agricultural geneticists and modern agribusiness, subsidized by the U.S. government to permit $5 pizza, is better than any terrorist plot to discombobulate the health and performance of the American people.

The Westman Diet

Dr. Eric Westman has been a vocal proponent of carbohydrate restriction to gain control over diabetes, as have Drs. Richard Bernstein, Mary Vernon, Richard Feinman, and Jeff Volek.

Several studies over the years have demonstrated that reductions in carbohydrate content of the diet yield reductions in weight and HbA1c (glycated hemoglobin, a reflection of average blood glucose over the preceding 60-90 days).

Among the more important recent clinical studies is a small experience from Duke University's Dr. Eric Westman. In this study, obese type 2 diabetics reduced carbohydrate intake to 20 grams per day or less: no wheat, oats, cornstarch, or sugars. Participants ate nuts, cheese, meats, eggs, and non-starchy vegetables.

After 6 months, average weight loss was 24.4 lbs, BMI was reduced from 37.8 to 34.4. At the end of the study, 95% of participants on this severe carbohydrate restriction reduced or eliminated their diabetes medications.

That was only after 6 months. Note that the ending BMI was still quite well into the obese range. Imagine what another 6-12 months would do, or achieving BMI somewhere closer to ideal.

Curiously, this idea of severe low-carbohydrate restriction to cure or minimize diabetes is not new. Sir William Osler, one of the founders of Johns Hopkins Hospital and author of the longstanding authoritative text, Principles and Practice of Medicine, advocated an diet identical to Dr. Westman's diet. So did Dr. Frederick Banting, discoverer of the pancreatic extract, insulin, to treat childhood diabetics. Before insulin, Banting and his colleagues at the University of Toronto used carbohydrate elimination (less than 10 g per day) to prolong the lives of children with diabetes.

This lesson was also learned many times during war time, when staples like bread were unavailable. The Siege of Paris in 1870 yielded cures for diabetes in many (or at least they stopped passing urine that tasted--yes, tasted--sweet and attracted flies), only to have it recur after the siege was over.

These are lessons we will have to relearn. As long as the American Diabetes Association and most physicians continue to advocate a diet of reduced fat, increased carbohydrate that includes plenty of "healthy whole grains," diabetics will continue to be diabetics, taking their insulin and multiple medications while developing neuropathy (nervous system degeneration), nephropathy (kidney disease and failure), atherosclerosis and heart attack, cataracts, and die 8 to 10 years earlier than non-diabetics.

All the while, we've had the combined wisdom from antiquity onwards: Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes.

(This applies, of course, only to adult overweight type 2 diabetics, not type 1 or some of the other variants.)

Handy dandy carb index

There are a number of ways to gauge your dietary carbohydrate exposure and its physiologic consequences.

One of my favorite ways is to do fingerstick blood sugars for a one-hour postprandial glucose. I like this because it provides real-time feedback on the glucose consequences of your last meal. This can pinpoint problem areas in your diet.

Another way is to measure small LDL particles. Because small LDL particles are created through a cascade that begins with carbohydrate consumption, measuring them provides an index of both carbohydrate exposure and sensitivity. Drawback: Getting access to the test.

For many people, the most practical and widely available gauge of carbohydrate intake and sensitivity is your hemoglobin A1c, or HbA1c.

HbA1c reflects the previous 60 to 90 days blood sugar fluctuations, since hemoglobin is irreversibly glycated by blood glucose. (Glycation is also the phenomenon responsible for formation of cataracts from glycation of lens proteins, kidney disease, arthritis from glycation of cartilage proteins, atherosclerosis from LDL glycation and components of the arterial wall, and many other conditions.)

HbA1c of a primitive hunter-gatherer foraging for leaves, roots, berries, and hunting for elk, ibex, wild boar, reptiles, and fish: 4.5% or less.

HbA1c of an average American: 5.2% (In the population I see, however, it is typically 5.6%, with many 6.0% and higher.)

HbA1c of diabetics: 6.5% or greater.

Don't be falsely reassured by not having a HbA1c that meets "official" criteria for diabetes. A HbA1c of 5.8%, for example, means that many of the complications suffered by diabetics--kidney disease, heightened risk for atherosclerosis, osteoarthritis, cataracts--are experienced at nearly the same rate as diabetics.

With our wheat-free, cornstarch-free, sugar-free diet, we have been aiming to reduce HbA1c to 4.8% or less, much as if you spent your days tracking wild boar.

Battery acid and oatmeal

Ever notice the warnings on your car's battery? "Danger: Sulfuric acid. Protective eyewear advised. Serious injury possible."

Sulfuric acid is among the most powerful and potentially harmful acids known. Get even a dilute quantity in your eyes and you will suffer serious burns and possibly loss of eyesight. Ingest it and you can sustain fatal injury to the mouth and esophagus. Sulfuric acid's potent tendency to react with other compounds is one of the reasons that it is used in industrial processes like petroleum refining. Sulfuric acid is also a component of the harsh atmosphere of Venus.

Know what food is the most potent source of sulfuric acid in the body? Oats.

Yes: Oatmeal, oat bran, and foods made from oats (you know what breakfast cereal I'm talking about) are the most potent sources of sulfuric acid in the human diet.

Why is this important? In the transition made by humans from net-alkaline hunter-gatherer diet to net-acid modern overloaded-with-grains diet, oats tip the scales heavily towards a drop in pH, i.e., more acidic.

The more acidic your diet, the more likely it is you develop osteoporosis and other bone diseases, oxalate kidney stones, and possibly other diseases.

Here's one reference for this effect.

What'll it be: Olive oil or bread?

We frequently discuss the advisability of consuming fats, carbohydrates, and various types within each category.

But what's the worst of all? Combining fats with carbohydrates.

Putting aside the wheat-is-worst form of carbohydrate issue and treating bread as a prototypical carbohydrate, let's play out a typical scenario, a make-believe feeding study in which a theoretical person is fed specific foods.

John is our test person, a 40-year old, 5 ft 10 inch, 210 lb, BMI 27.7 (roughly the mean for the U.S.) He starts with an average American diet of approximately 55% carbohydrates and 30% fat. Starting lipoproteins (NMR):

LDL particle number 1800 nmol/L
Small LDL 923 nmol/L


(The LDL particle number of 1800 nmol/L translates to measured LDL cholesterol of 180 mg/dl, i.e., drop last digit or divide by 10.)

Also, calculated LDL cholesterol is 167 mg/dl (yes, underestimating "true" measured LDL), HDL 42 mg/dl, triglycerides 170 mg/dl.

We feed him a diet increased in carbohydrates and reduced in fat, especially saturated fat, with more breakfast cereals, breads and other wheat products, pasta, fruit juices and fruit, and potatoes. After four weeks:

LDL particle number 2200 nmol/L
Small LDL 1378 nmol/L

Note that LDL particle number has increased by 400 nmol/L due entirely to the increase in small LDL particles triggered by carbohydrate consumption. Lipids show calculated LDL cholesterol 159 mg/dl--yes, a decrease, HDL 40 mg/dl, triglycerides 189 mg/dl. (At this point, if John's primary care doctor saw these numbers, he would congratulate John on reducing his LDL cholesterol and/or suggest a fibrate drug to reduce triglycerides.)

John takes a rest for four weeks during which his lipoproteins revert back to their starting values. We then repeat the process, this time replacing most carbohydrate calories with fats, weighed heavily in favor of saturated fats like fatty red meats, butter and other full-fat dairy products. After four weeks:

LDL particle number 2400 nmol/L


Let's

Chocolate peanut butter cup smoothie

Here's a simple recipe for chocolate peanut butter cup smoothie.

The coconut milk, nut butter, and flaxseed make this smoothie exceptionally filling. If you are a fan of cocoa flavonoids for reducing blood pressure, then this provides a wallop. Approximately 10% of cocoa by weight consists of the various cocoa flavonoids, like procyanidins (polymers of catechin and epicatechin) and quercetin, the components like responsible for many of the health benefits of cocoa.


Ingredients:
1/2 cup coconut milk
1 cup unsweetened almond milk
2 tablespoons cocoa powder (without alkali)
2 tablespoons shredded coconut (unsweetened)
1 tablespoon ground flaxseed
1 teaspoon almond extract
1 1/2 tablespoons natural peanut, almond, or sunflower seed butter
Non-nutritive sweetener to taste (stevia, Truvia, sucralose, xylitol, erythritol)
4 ice cubes

Combine ingredients in blender. Blend and serve.

If you plan to set any of the smoothie aside, then leave out the flaxseed, as it absorbs water and will expand and solidify if left to stand.

For an easy variation, try adding vanilla extract or 1/4 cup of sugar-free (sucralose) vanilla or coconut syrup from Torani or DaVinci and leave out the added sweetener.

The compromise I draw here is the use of non-nutritive sweeteners. Beware that they can increase appetite, since they likely trigger insulin release. However, this smoothie is so filling that I don't believe you will experience this effect with this recipe.

Letter from the insurance company

Claudia got this letter from her health insurance company:

Dear Ms. ------,

Based on a recent review of your cholesterol panel of January 12, 2011, we feel that you should strongly consider speaking to your doctor about cholesterol treatment.

Reducing cholesterol values to healthy levels has been shown to reduce heart attack risk . . .


Okay. So the health insurer wants Claudia to take a cholesterol drug in the hopes that it will reduce their exposure to the costs for her future heart catheterization, angioplasty and stent, or bypass surgery. This is understandable, given the extraordinary costs of such hospital services, typically running from $40,000 for a several hour-long outpatient catheterization procedure, to as much as $200,000 for a several day long stay for coronary bypass surgery.

So what's the problem?

Here are Claudia's most recent lipid values:

LDL cholesterol 196 mg/dl
HDL 88 mg/dl
Triglycerides 37 mg/dl
Total cholesterol 291 mg/dl

By the criteria followed by her health insurer, both total and LDL cholesterol are much too high. Note, of course, that LDL cholesterol was a calculated value, not measured.

Here are Claudia's lipoproteins, drawn simultaneously with her lipids:

LDL particle number 898 nmol/L
Small LDL particle number less than 90 nmol/L (Values less than 90 are not reported by Liposcience)

LDL particle number is, by far and away, the best measure of LDL particles, an actual count of particles, rather than a guesstimate of LDL particles gauged by measuring cholesterol in the low-density fraction of lipoproteins (i.e., LDL cholesterol). It is also measured and is highly reproducible.

To convert LDL particle number in nmol/L to an LDL cholesterol-like value in mg/dl, divide by ten (or just drop the last digit).

Claudia's measured LDL is therefore 89 mg/dl--54% lower than the crude calculated LDL suggests.

This is because virtually all of Claudia's LDL particles are large, with little or no small. This situation throws off the crude assumptions built into the LDL calculation, making it appear that she has very high LDL cholesterol.

Do you think that Big Pharma advertises this phenomenon?

Healthy smoothies

I've now seen several people who have either caused themselves to be diabetic or to have other phenomena associated with excessive consumption of carbohydrates, all by innocently indulging in a carbohydrate-packed smoothie every morning.

Kay, for instance, has a smoothie of a half-pint blueberries, a banana, a scoop of whey, low-fat yogurt, a cup of milk every morning. The rest of her diet was fairly healthy: salads with oil-based dressing for lunch, salmon and asparagus for dinner, only an occasional carbohydrate indulgence outside of her morning smoothie ritual. Yet she had a HbA1c (a reflection of prior 60 to 90 days average blood sugar) at the near-diabetic range of 5.9%.

The mistake most people make when making smoothies is relying too heavily on carbohydrates like fruit. A smoothie like the one made by Kay can easily top 50, 60, or 70 grams carbohydrates per serving, more than sufficient to send blood sugars up to 150 mg/dl or more.

So what can you put in your smoothie and not send you over the edge to diabetes, small LDL, and all the other undesirable phenomena of excessive carbohydrates? Here's a list:

--coconut milk, unsweetened almond milk. Less desirable: milk, full-fat soymilk
--ground flaxseed
--oils: flaxseed oil, coconut oil (melted), extra-light olive oil, walnut oil
--dried coconut
--extracts: vanilla, almond, coconut, cherry, hazelnut
--spices: cinnamon, nutmeg, ginger
--herbs: mint leaves, cilantro
--cocoa powder (unsweetened)
--nut or seed butters (peanut butter, almond butter, sunflower seed butter)
--tofu
--exotic ingredients (ingredients you wouldn't expect in a smoothie): spinach, kale, cucumber

How do you sweeten a smoothie? This is what trips up most people. If you resort to fruit like bananas, pineapple, or apple, you will readily send your blood sugar skyward. Honey, agave syrup, and sugar, of course, all increase blood sugar and/or have the adverse effects of fructose. Be careful of yogurt, also, for similar reasons.

Therefore, to sweeten your smoothie, consider:

--Small servings of berries, e.g., 8-10 blueberries, 2 strawberries, a few wedges of apple, half a kiwi
--Non-nutritive sweeteners like stevia, Truvia, sucralose, xylitol, erythritol. Also, sugar-free (sucralose-based) syrups like those from DaVinci and Torani are useful. (Just be aware that non-nutritive sweeteners can increase appetite--use sparingly.)

Also, note that, if you have divorced yourself from wheat, cornstarch, and sugars, your desire for sweet should be much reduced. Foods other people find just right will taste sickeningly sweet to you. You might therefore find that foods like peanut butter or coconut milk have a mild natural sweetness; added sweetness is only minimally necessary.

Coming next: I'll share a smoothie recipe or two of mine. Anyone want to share a recipe?

Insulin secretagogue

Dairy products have the peculiar property of triggering pancreatic release of insulin. The research group at Lund University in Sweden have contributed the most to documenting this phenomenon:




Mean (±SEM) incremental changes (?) in serum insulin in response to equal amounts of carbohydrate from a white-wheat-bread reference meal (x) and test meals of whey (?), milk (?), cheese (?), cod (?), gluten-low (?), and gluten-high (?) meals. From Nilsson 2004.

Note that it is the area under the curve (AUC), not the peak value, that assumes greatest importance.

Dairy products, especially milk, whey, and yogurt, are insulin secretagogues: they stimulate pancreatic release of insulin. The effect is likely due to amino acids and/or polypeptides in dairy products. (The effect is less prominent with cheese. Also see this study.)

By conventional wisdom, this may be a good thing, since the excess insulin will blunt the glucose rise after consumption. However, in my book, this is not such a good thing, since most of us have tired, beaten, overworked pancreatic beta cells from our decades of carbohydrate overconsumption. I fear that the effect of dairy products just take us a bit closer to beta cell failure: diabetes.

Good news: The effect is least with cheese.

Be gluten-free without "gluten-free"

While I've discussed this before, it is such a confusing issue that I'd like to discuss it again.

I advocate wheat elimination because consumption of products made from modern dwarf Triticum aestivum:

--Triggers formation of extravagant quantities of small LDL and LDL particle number (or apoprotein B)
--Triggers inflammatory phenomena like c-reactive protein, increases leptin resistance, and reduction of the protective adipocytokine, adiponectin.
--Encourages accumulation of deep visceral fat ("wheat belly") that is inflammatory and causes resistance to insulin
--Increases blood sugar more than nearly all other foods--higher than a Milky Way bar, higher than a Snickers bar, higher than table sugar.
--Is being linked to a growing number of immune-mediated diseases, including celiac disease (quadrupled over past 50 years), type 1 diabetes in children, and cerebellar ataxia and peripheral neuropathies.

This last group of wheat-related phenomena are primarily due to gluten, the collection of 50+ proteins found in each wheat plant. For this reason, people diagnosed with celiac disease are advised to eliminate gluten from wheat and other sources (barley, rye, triticale, bulgur) and to eat gluten-free foods.

Gluten-free has therefore come to be viewed as wheat-free and problem-free. It ain't so.

Among the few foods that increase blood glucose higher than wheat: cornstarch, rice starch, potato starch, and tapioca starch--Yup: the ingredients commonly used to replace wheat in gluten-free foods. They are also flagrant triggers of the small LDL pattern, along with increased triglycerides, reduced HDL, increased visceral fat, increased blood pressure. In short, gluten-free foods lack the immune and brain effects of wheat gluten, but still make you fat, hypertensive, and diabetic.

I tell patients to view gluten-free foods like jelly beans: Gluten-free pancakes, muffins, breads, etc. are indulgences, not healthy replacements for wheat. It's okay to have a few jelly beans now and then. But they should not be part of a frequent or daily routine. Same with gluten-free foods.
High-dose fish oil for Lp(a)

High-dose fish oil for Lp(a)

Lipoprotein(a), or Lp(a), is a problem area in coronary plaque reversal.

While our current Track Your Plaque record holder for largest percentage reduction in heart scan score has Lp(a), it remains among the more troublesome lipoprotein patterns.

One unique treatment for Lp(a) is high-dose omega-3 fatty acids from fish oil. While the data are relatively meager, there is one solid study from Lp(a) expert, Dr. Santica Marcovina of the University of Washington, called "The Lugalawa Study."

In this unique set of observations, 1300 members of a Bantu tribe living in Tanzania were studied. What made this population unusual is the fact that two groups of Bantus lived under different circumstances. One group lived on Nyasa Lake (3rd largest lake in Africa and reputed to have the greatest number of species of fish of any lake in the world) and ate large quantities of freshwater fish providing up to 500 mg of omega-3s, EPA and DHA, per day. Another Bantu group lived away from the lake as farmers, eating a pure vegetarian diet without fish.

Nyasa Lake












This situation among genetically similar stock provided a unique learning opportunity, a chance to assess whether different diets influenced Lp(a) levels.

The results: The fish-eating Bantus had an average Lp(a) level of 14.0 mg/dl. The farming, non-fish eating Bantus had an average Lp(a) of 27.0--a 48% difference. Curiously, a comparison of the apo(a) component of Lp(a) between the groups also showed that the fisherman expressed fewer dangerous small apo(a) forms, despite equal potential to express both.

The Lugalawa Study opens the question of whether similar results can be obtained not by moving to Tanzania and fishing Nyasa Lake, but by mimicking their experience by supplementing high doses of omega-3 fatty acids.

It's an intriguing question. In the Track Your Plaque program, we have no specific experience with this strategy, but it is certainly worth exploring further.

Watch for two upcoming Special Reports on the Track Your Plaque website in which we will be detailing 1)unique strategies for Lp(a) reduction, and 2) the usefulness of high-dose fish oil for coronary plaque reversal.

Interesting enough for a Virtual Clinical Trial?


Image courtesy Wikipedia.


Copyright 2008 William Davis, MD

Comments (16) -

  • Anonymous

    1/30/2008 1:22:00 PM |

    I have a Chinese friend that asked if Lp(a)is an inherited trait that Asians are known to have.  Are there races more likely to have Lp(a) than others?

  • Peter

    1/30/2008 2:41:00 PM |

    Hi Dr D,

    Thanks for the study, another very interesting one!

    You also have to consider that the fish must be displacing something from the diet of the vegetarian Bantu. By definition that means that there MUST be a reduction in vegetable intake. We know from hard intervention studies that a low fat diet automatically increases Lp(a) by 7% and adding copious fruits, vegetables and nuts makes the situation slightly worse (9% increase). Conversely a high fat diet reduces Lp(a) by 11%. The high fat diet was only 60% calories from fat and allowed 13% of calories as carbohydrate, so there is ample scope for less vegetables as a really radical intervention to drop Lp(a).

    Although not looking at Lp(a) the other hard intervention study looking at oxidative damage to lipids (and DNA and protein) found that near total elimination of all vegetables, without carbohydrate reduction, markedly reduced oxidative damage.

    When replacing veggies with fish it shouldn't surprise anyone that Lp(a) drops.

    Peter

  • Zute

    1/30/2008 3:45:00 PM |

    I'd finger grains as the culprit before before vegetables any day.

  • Neelesh

    1/30/2008 4:55:00 PM |

    Peter,
      The second study quoted has this logic:
    "Since no long-term effects of GTE were observed, the study essentially served as a fruit and vegetables depletion study.The overall effect of the 10-week period without dietary fruits and vegetables was a decrease in oxidative damage to DNA, blood proteins, and plasma lipids, concomitantly with marked changes in antioxidative defence."
        But the study did not have a group of people who were on a proper(TYP style?) fruit & veg diet to compare. So it sounds like "there were no long-term effects of GTE, but the diet was meat, so it must be the fruits and veggies that is the culprit". Or am I missing something?
    -neelesh

  • Dr. Davis

    1/30/2008 5:02:00 PM |

    RE: racial differences in Lp(a). Yes, there are distinct differences in Lp(a) levels and apo(a) size. Africans have the highest level. There are also pockets of incrased Lp(a) in the British/Irish/Scottish, some of  Jewish descent, among others. I do not know about Asian.

  • Peter

    1/30/2008 7:12:00 PM |

    zute, I'd blame grains for a host of problem but the low fat diet study doesn't give you menus, so who's to say. Except concluding that fruit, veg and nuts don't protect you from grains any more than they protect you from a reduced fat diet. Whichever. But the second study, which only looked at oxidative damage, was high in bread and cake. It's a pity they didn't look at Lp(a) in this one. I know which way I'd bet it went.

    Neelesh, I'm not quite sure I understand you comment. Are you suggesting meat inclusion alters the finding that fruit and vegetable elimination reduces oxidative damage? On a basic low carbohydrate, HIGH meat diet blood antioxidant status improves within three days. Again, this is far off of the topic of Lp(a), but meat got the credit for improving antioxidant status. You could equally well argue it was the lack of vegetables.

    I feel there is a massive difference between eating a steak on its own and eating that same steak with chips, peas, tomatoes, a bowl of green salad plus two bread rolls on the side. Intervention studies suggest one oxidises your lipids, the other doesn't. Epidemiological and observational studies are usually performed by people without this concept. In intervention studies veggies don't do so well. The authors are usually amazed. Very off topic (sorry) but there are very few intervention studies which measure Lp(a).

    Peter

  • Sasquatch

    1/30/2008 8:48:00 PM |

    Hi Peter,

    Interesting study.  Do you have any reason to attribute the increase in antioxidant defenses to increased meat consumption, rather than decreased carb?

  • Anonymous

    1/30/2008 8:57:00 PM |

    Hmmmmm...    I take high doses (5-6 grams) of High Potency EPA/DHA Fish Oil daily.

    I haven't seen any effect on my high Lp(a).

    Maybe it has to be directly from the fish (and while I do eat fish - it's only once or twice a week).

    Fruits and veggies - I eat a lot of those, too.

    Sheesh - this is confusing.  I can't imagine eating less fruits and veggies.

    Bonnie

  • Neelesh

    1/31/2008 2:58:00 AM |

    Peter,
      What I mean is this. Without a group of people being subjected to a fruit+veg+GTE diet and another group to meat+GTE group, one cannot conclude that "meat+GTE= less oxidation damage" implies  "lack of veg/fruit = less oxidation damage" .
        Again, this does not mean that there is no credit to the observation that meat+GTE reduced oxidation damage. However, we cannot logically deduce from that observation  "hence it is because of lack of fruits and veggies".

  • Anonymous

    1/31/2008 4:47:00 AM |

    High Lp(a) is one of the factors cited for the very high incidence of CVD in the South Asian population (India, Pakistan, Bangaldesh....).  Search Pubmed for work done by Dr. Enas Enas

  • Peter

    1/31/2008 6:15:00 AM |

    Hi sasquatch,

    I originally thought it was the lack of carbs rather than the high meat intake in the cyclist study, but the high carb vegetable washout study convinced me it was the lack of vegetables rather than carbs per se.

    The persistent antioxidant effect of fruit and veggies appears to be largely an effect of uric acid produced by ourselves in response to fructose. I've got a paper on this somewhere. Certainly the body eliminates most plant based antioxidants as fast as it can, ref the green tea extract paper.

    The Bantu on the lake eat roughly half a kilo of fish a day (300-600g/d). That's about 100g of animal protein and 550 kcal animal calories. Assuming a 2000 kcal food intake that's an awful lot of displaced vegetables. Results speak for themselves. As far as you can talk about results in an observational study.

    The paper linked to by Dr Davis provides this reference, which goes some way to explaining Bonnie's finding of no change in Lp(a) with fish oils. Unfortunately none of the fish (fish oil?) supportive refs have even abstracts on pubmed, so it's hard to see what's happening. BTW, I've got nothing against fish oils, 5g/d sounds like a very physiological intake. But it doesn't displace much in the way of vegetables.

    Peter

  • Peter

    1/31/2008 2:34:00 PM |

    Hi Neelesh,

    I think that the study concluded that the GTE  had no lasting effect beyond its excretion in the urine, with an elimination 1/2 life of 2 hours.

    There is no suggestion that meat plus GTE did any better than meat without GTE. It was a cross over study, so both groups got 3 weeks on GTE and 3 weeks off GTE.

    Their conclusion was that GTE supplementation made no difference to any measured parameter.

    As the GTE made no difference to antioxidant status (except transiently in the immediately post consumption period), the only hypothesis ultimately tested was whether fruit and veg elimination reduces oxidative stress.

    So comparing a meat plus GTE diet with a veg plus GTE diet is a little pointless.

    I would agree that you could argue that GTE does much more in the absence of meat, but I would want some logic as to how that might happen. I don't see why this should be the case.

    In this study we had a group of people acting as their own controls, drop the veggies, oxidation reduces, reintroduce the veggies, oxidation increases. Forget the GTE. It looks very simple to me, but then I'm a simple person.

    I as far as I can see the full text downloads for free. It does deserve careful reading. The EU was a major funder of the study and this funder was VERY unhappy with the results. From the EU's comments, linked to the asterisk at the end of the title, it looks to me as though the authors fought their funders tooth and nail to publish. It's a good study.

    Peter

  • promit

    8/31/2008 10:49:00 AM |

    I am a 34 year old male South Asian, who recently had a mild MI (troponin returned a negative, but my doctors confirmed an MI). Subsequently, I had an angiography which revealed an occlusion in the right coronary artery (RCA). All other fields (leftmain, LAD) etc were normal. I underwent a PTCA (coronary angioplasty) which opened up the block. I was not administered any stents, as the doctor felt that the thrombus would clear on its own.

    This was exactly 3 months ago. About 2 weeks ago, I went through a lipid profile test, along with some other tests the doctor prescribed (liver function test, Lp(a)). It was here that it was revealed that my Lp(a) was at 115 mg/dl. All along, all my risk factors were negative (blood pressure, blood sugar, lipids, and the only high figure was a marginally high cholesterol of 222). Finally, the doctor was able to put his finger on why this happened to me.

    He has now put me on Niacin, alongwith my statin (Tonact 20) and Clopivas tablets. I understand that Lp(a) is largely genetic, and not really fixable through lifestyle changes. I must mention that my cholestrol has come down to 94 from a value of 222 after I have been on medication, a healthy diet, and exercise, all of which I am maintaining with some rigor.

    I would like to know:

    1. Where do I stand on the Lp(a) thing? Is there anything I can do to help my cause? Just how bad is it? Am I unlikely to live very long, or develop further complications?

    2. Is it safe for me to have children? Will I be passing on this condition? What are the chances that my child will be unhealthy?

    3. I like to have a drink of beer occasionally. I have got a green signal from my doc a month or so ago to have the odd drink. Is it ok if its beer, and not wine, as he has recommended? Is it ok if I have  2 pints (each pint 330 ml) about 2-3 times a week?

    4. My Triglyceride levels are quite low (90). Also, my HDLC is currently at 30, and LDLC is 46, while VLDLC is 18. The LDLC/HDLC ratio is 1.53. Also CPK is 124 u/L. All other tests have returned normal values. F.B Sugar is 77 mg/dl. Fasting Urine Sugar is Nil. Blood Pressure is normal, I am not obese. There is no history of heart disease in the family known prior to this. I have quit smoking (I was a heavy smoker, about 20-30 cigerettes daily).

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