Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Friday, December 30, 2011

Histones deacetylation - new lead to degenerative diseases?

This recent article (and that paper) discuss the link between histones abnormality and schizophrenia.

Histones acetylation reduction or "deacetylation" cripples the ability of DNA to encode proteins thus can affects the entire cellullar metabolic and regenerative apparatus, producing effects probably resembling genetic disorders.  (What are histones? Read here)

The study reports particulary strong histone anomaly among schizophrenic patients of young age. This suggests a possible neurodegenerative process indicating a possible mechanism of the pathology of a young brain, that may lead to schizophrenia later in life.

Questions to think about:
  1. Could histone deacetylation anomaly lead to other common degenerative diseases?
  2. How does it affect mitochondria?
  3. Is there a connection between wheat histones (*) (or this) and human histones?
Few more facts about histones and neurological health:

- Since acetylation reduction is done by deacetylation enzymes called "deacetylase", inhibiting of deacetylase should restore the required level of histone acetylation. What are the common deacetylase inhibitors? Quote from the wiki article:

HDIs [Histone Deacetylase Inhibitors] fall into several groupings, in order of decreasing potency[6]:
  • hydroxamic acids (or hydroxamates), such as trichostatin A,
  • cyclic tetrapeptides (such as trapoxin B), and the depsipeptides,
  • benzamides,
  • electrophilic ketones, and 
  • the aliphatic acid compounds such as phenylbutyrate and valproic acid.

More references:
Scientists discover a brain cell malfunction in schizophrenia
( Note: the link above as well as the original article twit was posted on this blog )

Note (*): interestingly, wheat uses histone disruptors to fight funghi.  New wheat variety introduced in the last century was specifically bread to resist funghi and molds.  Recent wheat variety  = heart diesease and cancer.  Earlier wheat, 19-th century and back = no prob!  Or is it too far out to conclude that?

Latest news (9-Feb-2012):

Scientists make discovery related to atherosclerosis

A research team funded by the National Science Council achieved a breakthrough in molecular--targeted therapy of atherosclerosis by experimenting on the condition’s formation mechanism from the perspective of cardiovascular biodynamics.
The council said discoveries by the team led by National Health Research Institutes [Taiwan] researcher Chiu Jeng-jiann (裘正健) had been recognized by the prominent academic journal Physiological Reviews in a cover story last year.

...the team focused on discovering the mechanism of how different levels of blood flow shear stress could affect molecules related to atherosclerosis formulation. The team was able to demonstrate that oscillated shear stress can increase the performance of several types of histone deacetylase (HDAC) in the endothelium, modulating some transcription factors and gene transcription. A noteworthy discovery is that the third type of HDAC has the important function of modulating oxidation, inflammation and hyperplasia and can be seen as an important targeted therapy for the prevention or treatment of atherosclerosis, Chiu said.

"Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives", JENG-JIANN CHIU AND SHU CHIEN, Physiol Rev 91: 327–387, 2011

Update (28/08/2013)

Age-Related Forgetfulness Tied to Diminished Brain Protein (RbAp48)


RbAp48 belongs to the histone deacetylase complex that associates with the retinoblastoma protein.


Sunday, December 11, 2011

More starch more breast cancer recurrence

New analysis based on WHEL study titled "Starch Intake May Influence Risk for Breast Cancer Recurrence" presented at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium, held Dec. 6-10, 2011.


“The results show that it’s not just overall carbohydrates, but particularly starch,” said Jennifer A. Emond, M.S., a public health doctoral student at the University of California, San Diego. “Women who increased their starch intake over one year were at a much likelier risk for recurring.”
Researchers conducted a subset analysis of 2,651 women who participated in the Women’s Healthy Eating and Living (WHEL) Dietary Intervention Trial, a plant-based intervention trial that enrolled about 3,088 survivors of breast cancer. WHEL researchers studied breast cancer recurrence and followed the participants for an average of seven years.
The change in starch intake was “independent of dietary changes that happened in the intervention arm,” Emond said. “It is independent of more global changes in diet quality.”

I have to comment on the following quote: . “The WHEL dietary trial, even though it focused on fruits and vegetables, fiber and fat, didn’t really have a specific carbohydrate goal,” Emond said.

Time and time again studies focus on some secondary issues such as which particular vegetable or fruit selection affects some outcome while at the same time ignoring a major issue of macronutrient ratios! Such analyses often come as afterthoughts and end up using incomplete or partial data, just because the study proponents didn't bother to measure a major variable.  Now they seem surprized finding an "elephant" in their  lab! The biggest kicker is that vegetables - the one "healthy" diet aspect that they WHEL study authors did focused to the detriment of other more real issues, turned out to be irrelevant as far as cancer was concerned! (see the study I discuss further down)

Even though the results suffer from the fact that the original study methodology wasn't properly focused on the issue that mattered, the results are consistent with other studies. For example this one:

"Carbohydrates and the Risk of Breast Cancer among Mexican Women"
Isabelle Romieu, Eduardo Lazcano-Ponce, Luisa Maria Sanchez-Zamorano, Walter Willett and Mauricio Hernandez-Avila

The study showed a very strong breast cancer promoting effect of carbohydrate consumption: for every additional 1% of carbohydrate calories consumed above 52%, the relative risk of breast cancer was incrementally increasing by about 10%!

Consistent also with the Italian data:

"Dietary glycemic index, glycemic load, and the risk of breast cancer in an Italian prospective cohort study", Sabina Sieri et al.

The study showed that a 56% higher glycaemic load (from 96g/d to 150g/d) produced 2.53 times higher relative risk of breast cancer among Italian women.


The following paper (also based on the same WHEL study as the headline study!) demonstrated that a low fat high vegetable diet was useless for fighting cancer!

"Influence of a Diet Very High in Vegetables, Fruit, and Fiber and Low in Fat on Prognosis Following Treatment for Breast Cancer." John P. Pierce, PhD; Loki Natarajan, PhD; Bette J. Caan, et al. The Women's Healthy Eating and Living (WHEL) Randomized Trial. JAMA. 2007;298:289-298.

Among survivors of early stage breast cancer, adoption of a diet that was very high in vegetables, fruit, and fiber and low in fat did not reduce additional breast cancer events or mortality during a 7.3-year follow-up period.


Similar pattern with the ovarian cancer:

"Nutrient dietary patterns and the risk of breast and ovarian cancers." Edefonti V, et al., Int J Cancer. 2008 Feb 1;122(3):609-13.

... Cases were 2,569 breast cancers and 1,031 ovarian cancers hospitalized in 4 Italian areas between 1991 and 1999. Controls were 3,413 women from the same hospital network. Dietary habits were investigated through a validated food-frequency questionnaire. ... The animal products pattern and the unsaturated fats pattern were inversely associated with breast cancer (OR = 0.74, 95% CI: 0.61-0.91 and OR = 0.83, 95% CI: 0.68-1.00, respectively, for the highest consumption quartile), whereas the starch-rich pattern was directly associated with it (OR = 1.34, 95% CI: 1.10-1.65). The vitamins and fiber pattern was inversely associated with ovarian cancer (OR = 0.77, 95% CI: 0.61-0.98), whereas the starch-rich pattern was directly associated with it (OR = 1.85, 95% CI: 1.37-2.48). In conclusion, the starch-rich pattern is potentially an unfavorable indicator of risk for both breast and ovarian cancers, while the animal products and the vitamins and fiber patterns may be associated with a reduced risk of breast and ovarian cancers, respectively.

[side issue: carbs and HDL putting it here as a reminder for myself to write some more on it]
"Carbohydrate intake and HDL in a multiethnic population." Am J Clin Nutr. 2007 Jan;85(1):225-30.

"Previous research has identified ethnic differences in cholesterol and other blood fat levels that couldn't be explained by genes, obesity, lifestyle factors or diet, Merchant and his team note, but these analyses usually looked at dietary fat, not carbohydrate consumption"

Another Italian study, similar pattern:

"Intake of macronutrients and risk of breast cancer."
Franceschi S, Favero A, Decarli A, Negri E, La Vecchia C, Ferraroni M, Russo A, Salvini S, Amadori D, Conti E, Montella M, Giacosa A.
Lancet. 1996 May 18;347(9012):1351-6.

... FINDINGS: The risk of breast cancer decreased with increasing total fat intake (trend p ? 0.01) whereas the risk increased with increasing intake of available carbohydrates (trend p=0.002). The odds ratios for women in the highest compared with the lowest quintile of energy-adjusted intake were 0.81 for total fat and 1.30 for available carbohydrates. Starch was the chief contributor to the positive association with available carbohydrates. ... Conversely, the intakes of saturated fatty acids, protein, and fibre were not significantly associated with breast-cancer risk. ...


Update (25-12-2011)

I am slapping this paper here quickly for the reference although it is not strictly on-topic (thanks Kiran)

Mean life span of CR sucrose-fed rats was significantly greater than all other groups [including starch fed CR]

Feed Corn starch Sugar
100% cal  
60% cal

The rats diet consisted of 14% protein, 10% fat, and 66% sucrose or cornstarch. The numbers are the average lifespans of rats in days (standard deviation is about +/-20days). 100% cal means an ad-libidum diet. 60% cal = calorie-restriction diet.
(this study needs a discussion)

Thursday, December 1, 2011

Arterial plaque = glucose + insulin, C14 traced study

Atheroma (from wiki)

A "blast from the past": two old forgotten papers that were never followed up, as far as I was able to find.  I wonder why not?


R. W. Stout, Lancet p702,1968


Discussion (p1 of 2)
Discussion (p2 of 2)


R.W. Stout, Lancet p467,1969

Discussion (p1 of 2)
Discussion (p2 of 2)

Dav0 found a more recent paper by Stout (thanks):

Insulin and Atheroma: 20-Yr Perspective, Robert W Stout, MD, DSc, FRCP


Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower highdensity lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels.


Monday, November 7, 2011

Alzheimer's: The detrimental role of a high carbohydrate diet

Interesting paper just published:
"Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet", S.Seneff, G.Wainwright, L.Mascitelli, European Journal of Internal Medicine 22 (2011) 134–140.

"A ketogenic diet has been found to be therapeutic in AD patients [72,73]. It involves an extremely high fat diet, with up to 88% of calories derived from fats. This benefit may be likely due in part to the bioavailability of a plentiful supply of fats to repair damaged membranes. However, this diet leads to the generation of a significant concentration of ketone bodies in the blood serum, which can be used as an alternative fuel to glucose ..."

A very good and brief summary by Ted Hutchison is here (TUESDAY, 11 OCTOBER 2011).

Tuesday, October 4, 2011

Is t2 diabetes result of mitochondrial destruction?


1. A hypothesis:

- Metabolic syndrome and diabetes t2 results from mitochondrial destruction caused by overfeeding with glucose (and fructose but only in the liver), taking place over many years. An individual mitochondrion has (hypothetical assumption!) a fixed maximal total energy yield out of the two main energy sources: glucose (or glucose+fructose in the liver) plus fatty acids.

There is a self-clamping regulatory mechanism preventing mitochondrial overfeeding by fatty acids, by means of Malonyl-CoA/CPT1 feedback (see Peter’s discussion), but there are no very effective self-regulation feedbacks for glucose, only a partial mechanism reducing the glucose transport into in the cells! This partial mechanism is mediated by insulin regulating the transport of glucose into a cell through the cellullar membrane. This regulatory mechanism is not always effective or fast because the insulin secretion is not local to the cell, rather it is produced in the pancreas whose rate of secretion is regulated by the autonomous nervous system and pancreating glucose concentration involving many factors other than some particular mitochondria overload. Furthermore, the insulin regulation (blocking) of glucose can be overriden by high glucose concentration.

2. Conclusions.

A straight conclusion would be that a high carbohydrate diet can indeed be healthy and avoid diabetes as long as it restricts calories to prevent mitichondrial overfeeding. What is the limit? In my guesstimate (based on published literature) - probably around 25kcal/kg for women and 30kcal/kg for men.

A second straight conclusion is that a high fat low carb diet automatically avoids mitochondrial deterioration and thus diabetes among other degenerative diseases, by its built-in biochemical overfeeding protection mechanism. (note: my daily caloric intake on a high animal fat diet, is and has been around 20-25kcal/kg since 1999).

A third conclusion concerns a situation of the cells with the insufficient number of or worn-out mitochondria. Having lower total mitochondrial energy throughput, such cells may be forced to over-rely upon and and over-utilize the Penthose Phosphate Pathway (PPP) (also called the Penthose Shunt) which takes place in the cytosol volume outside of the mitochondria. This has originally been proposed by Dr. Jan Kwasniewski, the author of Optimal Diet in the 1970-ties. I found his idea fascinating, largely because there was no easy or obvious way of proving it at the time, and last but not least - it flew right against the medical dogma! Interestingly the PPP is mainly a synthesis pathways resulting in lipids and lipoproteins manufactured inside the cells, in-situ. Such as the infamous "cholesterol" plaque perhaps? Out of glucose? Like suggested by R.W. Stout in his 1968 and 1969 Lancet papers?

--- Part 2 (9-Oct-2011) ---

3. Declining energy syndrome and carbo-loading trap.

More conclusions can be drawn out of this simple hypothesis. If t2 diabetes is the results of mitochondrial decline caused by overfeeding (carbs or by a combination of carbs and fats) then it should be accompanied by a steadily declining energy yield.

Suppose for the sake of discussion that a healthy individual consumes 30kcal/kg/day, leading active live. If he looses 10% of his mitochondria he would be able to process only 27kcal/kg/day. Less energy to work, more lethargic, getting tired sooner. What do we do when that happens? I was in that situation 15 years ago. Falling energy level at work, especially after 3pm. I snacked! I snacked on carbs! Why on carbs? Because I couldn't snack on fat! (even if I didn't believe that fat is harmful...) Fats don't work if you have mitochondrial deficiency because of the Malonyl-CoA/CPT1 feedback(*). A mitochondrion can only process a certain maximum amount of energy out of fat and that's it! If your total mitochndrial yield declined from 30 to 27 during the first 20 years of dietary abuse, then 27 is all what you can get out of fat! But you can still push your partially worn-out "engine" into overdrive by flooding it with extra glucose! It will sputter and spew out lots of smoke polluting your cells with free radicals, AGE's etc but it would allow you to bring your yield back to the previous level of 30. At least for a time being because the process of mitochondrial decline has accelerated due to the pushing them over the limit and the ensuing end product toxicity. So instead of 27kcak/kg/d, now the maximum available yield drops by another 10%, this time over 2 years. You can now safely draw 24kcal/kg/d out of fat or carbs or a combination of both. However if you want to stay awake at work you have got to load up on carb snack now by 20% not 10% over your maximum limits creating more problems, requiring a lot more insulin to overcame the natural barrier that your body cells have enacted against your plan. It also requires maintaining a high blood glucose level to speed up diffusion across cellular boundaries. Which particular cells of your body will be the first in line to see the high glucose and high insulin? Your arterial endothelium! Your liver!

This appears to be a run-away process where your tissues cells would keep enacting more and more barriers agaisnt excessive metabolism, your conscious brain will make you snack like crazy on carbs to maintain the same energy level, your pancreas will try keeping up with that pumping your insulin, your immune system will work overtime trying to clean up the mess after glucose and eventually it will also try saving your body tissue by attacking the source of the excessive insulin - pancreating beta cells, in some cases it will try even to sequester the excessive insulin floating in your bloodstream, and last but not least your poor mitochondria will keep dying! Eventually one of more of the players described above will give up. If you stop snacking and keep below your maximum metabolic yield, you will feel hungry and lethargic. Especially if you have to work 9-5. If you don's stop snacking your blood glucose would go up until you develop kidney failure. If you force you blood glucose below renal dumping threshold (about 160mg/dl) by injecting insulin you will develop heart failure or arteriosclerosis (or both). What to do? This will be the next subject.

4. The way out - what exactly happens (and when) if you start curing yourself of diabetes using a high fat low carb diet.

More references, links and thoughts are in this file.


*) I am speculating but there seems to be cases when the fat-clamp mechanism may also be defeated, leading to fatty acids overload(+). This condition is also harmful creating large amount of toxins that require a massive cleanup operation my the immune system (see Masterjohn's article, in my reference file above). I suspect that this is one reason behind the so-called "low-carb flu" syndrome sometimes reported by inexperienced diabetic low carb dieters. It is interesting that fat overload (if that does happen, however unlikely) may be as unpleasant as glucose overload!

Footnote to a footnote:

+) Indeed it does happen! Peter just posted an interesting discussion about this issue here. A must read! It appears that when the adipose tissue develops insulin resistance, it is then capable of releasing fat into triglyceride particles and into the bloodstream under the condition of falling but still higher than normal insulin level! Fatty acids are then forced into the cells and a smaller fraction are then forced into mitochondria. The free fatty acids left-over inside the cell (but outside of the mitochondria) become the main cause of the insulin resistance and the cause of major cellullar cleanup operation. I have a mental picture of my old sputtering "Komar" motorbike with its carburator overflooded with gasoline...

This makes a fascinating fork in the metabolic failure modes under overfeeding. On one hand, the overfeeding with glucose may be wearing off the mitochondria and also forcing the excess fuel into adipocytes. On the other hand releasing those excessive fats from the adipocytes into the bloodstream may be setting up the physiological insulin resistance and still damaging the cells even more through the high free fatty acids level in the cytosol. Interestingly this excessive fatty acids may as likely (if not more so) come from the internal source (adipose tissue) than from a diet! It also explains why many obese people experience a health breakdown only AFTER they undergo a weight loss, especially after a repeatable weight loss and weight gain cycling.

A weight loss diet is therefore ALWAYS a HIGH FAT diet even if a person eats nothing but lean veggies!

--- Part 3 (15-Oct-2011) ---

The reason I am considering this mitochondrial decline model seriously is because of my experience. Back in July 1999 when I started my low carb high animal fat diet (almost by accident) I did experience a noticeable lack of energy, light-headedness and dizziness for a couple of weeks. Also: low blood pressure and reduced blood clotting that showed up by excessive and random bruising on my hands.
The worst part of it (dizziness and weakness) last only for 2 weeks. I didn't have diabetes just metabolic syndrome and hypoglycemic episodes. In my case, I was able to combat those initial low carb startup difficulties by carrying with me some high fat snacks such as Swiss cheese, Polish saussage and nuts.

The main problem is: when you stop consuming excessive carbohydrates then your damaged mitochondria might not be able to deliver enough energy out of fat and carbs to sustain your previous energy expenditure. You do feel the loss of energy immediately, and more hunger, therefore:    You must slow down!

 The only way for your mitochondria to recover or for your tissue to stop deteriorating and then regenerate(**) is to maintain the lower caloric intake compatible with your maximal mitochondrial yield. It will recover! This is the good news. The bad news is that it will take a few years!

**) I am not sure if mitochondria can individually regenerate by themselves or if the only way is for the body to regrow the new cells from stem-cells.

Yes to both, see this comment by Dr. Jack Kruse, on Peter's blog.
The low carb high fat therapy can be divided into 3 stages.

a) Switch-over

This is when the initial difficulty will show up. For diabetics and elderly this could be severe enough to warrant some medical supervision. Your body, digestive system and metabolic apparatus is switching over from carbohydrates to animal fats as the main energy source. There are hundreds of grams of enzymes circulating in your system that are no longer needed and have to be disposed off. Enzymes are protein. you will excrete their end products in urine, during this stage. Ketone bodies will show up in urine since your liver will be producing them more than your body tissue are able (yet) to utilize as fuel. Fortunately ketones in urine are in this case inconsequential but one has to be aware of it because of the rampant scare-mongering propagated by some uninformed people. I have seen many cases of people being scared by ketones and abandoned a low carb high fat diet, to their detriment. This stage last typically from 2 week to 2 months.

b) Rapid at first, then gradual improvement, disappearance of most chronic disease symptomes.

At this stage, most diabetic patients will experience disappearance of all or of most of the symptoms. Also, other chronic disease will show a lesser or stronger reversal, for example: auto-immune diseases, chronic intestinal diseases, arteriosclerosis, cardiac diseases, vascular diseases, neurological etc. However, the energy level may still be lower than on the standard high carb high caloric diet. Good news is that this yield will no longer be deteriorating. It will begin to slowly improve.

Many changes will take place at this stage, for example:
  • Eating and snacking habits will be completely modified.
  • Hunger will disappear, one will have to eat only once or twice a day. There will be no "toxic" hunger!(***) Total caloric intake will automatically and painlessly come down by about 30%, compared with the previous high carb nutrition. Please notice how close this ties with the Caloric Restriction programme! The low carb high fat diet is the Caloric Restriction program without hunger! For diabetic patients, all symptoms should disappear during this period. Most patients (except dm t1) will no longer need diabetic drugs or insulin. However - if they go back to a high carb diet, their diabetes will return.
  • Breathing rate will go down. An interesting side effect will be an ability to free-dive for a longer periods of time due to lower carbon dioxide release per calorie due to fat oxidation chemistry and due to an overall lower energy expenditure!.
  • Ability to better withstand cold temperature and cold weather.
  • Greater resistant to stress and alleviation of some neurological disorders, mood disorders, bad temper etc. This is a big and important effect! The low carb high fat metabolism is accompanied by a significantly different endocrine reaction against stress stimuli. A stress will no longer trigger a "panic paralyzis" reaction or initiate a panic attack, but will instead stimulate a generally pleasant and always useful rush of energy! The effects of stress hormones upon the neural tissues will be much less harmful in the presence of ketone bodies as in ketogenic diet, than in their absence as is more typical under the high carb diets in metabolic syndrome.  Ketone bodies are not produced when insulin and glucose levels are too high! More on the effect of stress hormones, ketone bodies and glucose upon the neural tissue is discussed here.
  • Greater resistant against infections, viral and bacterial. No more seasonal flu!
  • Complete prevention of tooth decay and dental plaque. I have seen cases of molar teeth broken in half self-healed by sealing off of the cleavage.
  • Improved cholesterol level and profile.  One notable exception: patients with fatty liver disease, the level of LDL may climb to a very high value, I have seen as high as 700md/dl sustained over a couple of years. No adverse health impact, other than scaring a "beejesus" out of some doctors... . Note that after the fatty liver recovers, LDL comes down.
  • Lower capacity to tolerate a once off high carbohydrate meal (or high intake of alcohol).  At this stage, people with metabolic syndrome and diabetics must still be careful to actually measure their daily intake of carbs and ensure it is within the strictly limited band. Typically about 50g per day.   Failure to observe this limit results in unpleasant symptoms and is hazardous to one's health.

***) The term "toxic hunger" as coined by Fuhrman, is in my opinion probably related to a falling level of glucose and insulin from a high value below the level sufficient to sustain glucose metabolism (in metabolic syndrome) but still too high to allow burning of one's body fat. This leads to a condition where some or all body tissues are temporarily starved of energy.   In a non-diabetic, insulin and glucose levels do not go too high thus insulin can quickly go down in between the meals prompting the release of the stored body fat.

High insulin = low leptin = burning glucose not fat.
Low insulin = high leptin = burning fat not glucose.

A very weak feeling of a slight hunger under ketogenic body fat "burning" can be easily overcome or forgotten, and is totally different from a "panicky" acute and almost painful hunger pangs experienced by diabetics and people with metabolic syndrome.  

c) Long term recovery

After several years on the low carb high fat diet, one's energy level will gradually come back to the previous level (like in one's 30-ties). This is probably due to tissue regeneration from stem cells. In my experience this will take a minumum of 7 years. An ability to tolerate a once-off higher intake of carbohydrates (typ. up to 150g) will come back at this stage. People who had diabetes may probably (I am hypothesizing) be able to come back to some kind of medium carb medium caloric diet if they wanted to, without getting diabetes because they will no longer be insulin resistant.

A must-read:
"Metabolic flexibility and the identical twins"


Saturday, September 24, 2011

How Our Genes Respond to the Foods We Eat

Interesting and important research coming from Berit Johansen,Ingerid Arbo, Hans-Richard Brattbakk et al., from the Norwegian University of Science and Technology (note *):

Feed Your Genes: How Our Genes Respond to the Foods We Eat


If you could ask your genes to say what kinds of foods are best for your health, they would have a simple answer: one-third protein, one-third fat and one-third carbohydrates. That's what recent genetic research from the Norwegian University of Science and Technology (NTNU) shows is the best recipe to limit your risk of most lifestyle-related diseases.

NTNU researchers Ingerid Arbo and Hans-Richard Brattbakk have fed slightly overweight people different diets, and studied the effect of this on gene expression.

"We have found that a diet with 65% carbohydrates, which often is what the average Norwegian eats in some meals, causes a number of classes of genes to work overtime," ... "This affects not only the genes that cause inflammation in the body, which was what we originally wanted to study, but also genes associated with development of cardiovascular disease, some cancers, dementia, and type 2 diabetes -- all the major lifestyle-related diseases," she says.

"Both low-carb and high-carb diets are wrong," says Johansen. "But a low-carb diet is closer to the right diet. A healthy diet shouldn't be made up of more than one-third carbohydrates (up to 40 per cent of calories) in each meal, otherwise we stimulate our genes to initiate the activity that creates inflammation in the body." This is not the kind of inflammation that you would experience as pain or an illness, but instead it is as if you are battling a chronic light flu-like condition. Your skin is slightly redder, your body stores more water, you feel warmer, and you're not on top mentally. Scientists call this metabolic inflammation.

It was not only inflammatory genes that were putting in overtime, as it would turn out. Some clusters of genes that stood out as overactive are linked to the most common lifestyle diseases.
"Genes that are involved in type 2 diabetes, cardiovascular disease, Alzheimer's disease and some forms of cancer respond to diet, and are up-regulated, or activated, by a carbohydrate-rich diet," says Johansen.

"We're not saying that you can prevent or delay the onset of Alzheimer's if you eat right, but it seems sensible to reduce the carbohydrates in our diets," she suggests.

The immune system operates as if it is the body's surveillance authority and police. When we consume too many carbohydrates and the body is triggered to react, the immune system mobilizes its strength, as if the body were being invaded by bacteria or viruses.
"Genes respond immediately to what they have to work with. It is likely that insulin controls this arms race," Johansen says. "But it's not as simple as the regulation of blood sugar, as many believe. The key lies in insulin's secondary role in a number of other mechanisms. A healthy diet is about eating specific kinds of foods so that that we minimize the body's need to secrete insulin. The secretion of insulin is a defense mechanism in response to too much glucose in the blood, and whether that glucose comes from sugar or from non-sweet carbohydrates such as starches (potatoes, white bread, rice, etc.), doesn't really matter."

Johansen has some encouraging words, however, for those of us who have been eating a high carbohydrate diet. "It took just six days to change the gene expression of each of the volunteers," she says, "so it's easy to get started. But if you want to reduce your likelihood of lifestyle disease, this new diet will have to be a permanent change."

The best is to cut down on potatoes, rice and pasta, and to allow ourselves some of the good stuff that has long been in the doghouse in the refrigerator.
"Instead of light products, we should eat real mayonnaise and sour cream," Johansen says, "and have real cream in your sauce, and eat oily fish.

Fountain-of-youth genes

Johansen's research also shows that some genes are not up-regulated, but rather the opposite -- they calm down rather than speed up.

"It was interesting to see the reduction in genetic activity, but we were really happy to see which genes were involved. One set of genes is linked to cardiovascular disease. They were down-regulated in response to a balanced diet, as opposed to a carbohydrate-rich diet," she says. Another gene that was significantly differently expressed by the diets that were tested was one that is commonly called "the youth gene" in the international research literature.
"We haven't actually stumbled on the fountain of youth here," Johansen laughs, "but we should take these results seriously. The important thing for us is, little by little, we are uncovering the mechanisms of disease progression for many of our major lifestyle-related disorders."

(I wish to express my thanks to chili_in_a_can from McDougall's vegan forum for publishing the article link)


Contact: Berit Johansen, Department of Biology, NTNU
TEL. +47 73 59 86 91 E-MAIL: berit.johansen at bio dot ntnu dot no

More articles on this topic:

What should we eat to stay healthy?

Best diet: One-third protein, carbs, fat


*) Note the effect this article may have had in Norway, recently (December 2011): link


Thursday, September 8, 2011

Destruction of economy by parasitic governments and financial institutions


The destruction of our economy by parasitic governments and financial institutions


Most countries’ financial centers and governments are currently in the process of expanding the supply of world currencies and cheap credit, in order to boost their own budgets, salaries and political power and to avoid recessions.   One of the effects of this policy is the protection of their own personal wealth consisting of paper assets such as bond and stock funds that would otherwise have collapsed.


A similar expansion of the monetary supply has historically led to the de-industrialization of  entire regions or countries that followed such policies for a sustainable period of time, typically over several generations.   On the surface, the mechanism of such de-industrialization seems to work by inflating the costs of doing business faster than the price inflation of manufactured goods and services produced by affected companies, thus destroying profitability, especially when a vast supply of goods is available from peripheral provinces or from other countries.  One such example was the 5th century Roman Empire (see Fall Of Empire essay), the other one is 16th century Spain under Philip II.

“Nuts and bolts”

Industrial companies that may initially enjoy the cheap credit, use it to expand production facilities or other business assets, which then leads to excess production or excess supply of services and inevitably destroys profitability.   Decreasing profitability reduces investment yield, the Return On Investment (ROI) but it also serves to restrain the inflationary pressure fuelled by the financial expansion.   The reduced inflationary pressure due to collapsing profitability allows the central banks and governments to maintain the low inter-banking lending interest rate which in turn facilitates the issuance of even more credit, including borrowing by the governments for virtually limitless spending on themselves.

Risk management, CDS and leverage

The issuance of more and more credit to an expanding circle of corporate and other borrowers at a time of falling yields would have normally been stopped at some level by the rising risk premium preventing a further reduction of interest rates.  Rising loan risk would have acted as a negative feedback preventing the currently observed unprecedented drop in interest rates and related bond yields.  It would have ultimately prevented excessive credit generation.   The negative risk-mediated feedback has been sabotaged by the use of a special form of financial credit insurance called “Credit Default Swaps” (CDS).   CDS allowed the lending institutions to exceed the lending limits imposed by the normal risk avoidance standards (and by common sense) , by allowing them to profitably lend, giving very low and falling loan interest rates.   In this low interest rate environment, it was necessary to lower the required capital reserve for banks and financial institutions such as hedge funds in order to maintain the expected profitability.  Until recently, this required capital reserve was decreed to be 1:11 (capital-to-total loans), which was recently further reduced by the “Basel 3” agreement to 1:30 bringing the world banks to similar “standards” as hedge  funds which “enjoyed”  the 30:1 leverage even before the 2008 crash  (Leverage is the inverse of the capital requirement).

Positive feedback loop of destruction

Apart from destroying industrial profits, the excessive credit also creates bubbles in selected investment sectors such as stock, futures and bonds.  Rising bond prices are further depressing  the yields and interest rates which further accelerated the lending.  This situation is described in science and engineering by the term “positive feedback loop”. This means that even a small input stimulus is amplified by the system and fed back to an input, amplifying itself further until the system reaches some very large deviation from an equilibrium, and saturates or the system breaks down.

Eventually financial companies flee the market where interest rates and Return On Investment (ROI) has been depressed, moving most of their investment capital off-shore to countries where the ROI is still high.   The process is repeated until all manufacturing economies end up eventually running unprofitable industries, subsidized at first by the investment capital influx, later by government subsidies to maintain employment and to prevent the paper assets backed by industry from crashing.   Subsidized manufacturing in poorer countries floods the world market with underpriced industrial goods allowing prices of industrial goods to remain stagnant (deflation) in spite of the rapid expansion of the financial system and money.
I saw the future...
The last stage of this economic destruction is the breakdown of the unprofitable manufacturing, resources and agricultural sectors when the subsidies run out or when the employees refuse to work under the austere conditions imposed upon them by the profit squeeze. This process, like the credit growth itself, is also governed by the positive feedback law.   Once started, it will accelerate, fuelling itself like a cancer or fire.  This will happen specifically, when food prices and the cost of living overtake the wages paid by unprofitable manufacturing companies causing industrial disruption due to strikes and closures, leading to further increases in the cost of living and so on.   

The impact of this upon the developed countries that almost totally depend upon the subsidized under-priced production from the developing countries, will be equally severe.  A decline of the subsidized imports of industrial and consumer goods will cause the supply chain to break down in the developed economies, leading to explosive inflation of all prices for manufactured goods, commodities, food and services.  The ensuing inflation will put an upward pressure on interest rates which government will no longer be able to obfuscate or manipulate using financial techniques alone.


The  inflation-induced jump in interest rates and yields will crash the bond market (bond values are inverse to their yields).  Old bonds will drop in value destroying most of the pension funds and probably most of the financial institutions, given that it may trigger an avalanche of CDS claims (another positive feedback) which will accelerate the institutional and systemic collapse.  At the same time, the new bonds will become very expensive for borrowers to issue, thereby derailing the “gravy train” enjoyed by governments and large corporations the world over.  It may even make the refinancing or rollover of old debt impossible.

The break-down of the government bond market will cause currency exchange rates to vary wildly and may cause some currencies to crash and disappear, beginning with those countries that will default on their government bonds first and ending with probably all presently known paper currencies disappearing and being replaced by something else.  

Science, technology and ideas (including business ideas) are unlimited.   Completely new industrial companies, technologies and services will be created, filling in the present business vacuum, using new-old forms of self-financing and capital-rising that are more robust and do not depend on large financial institutions and governments.  This will happen in the countries that  provide a legal framework effective in protecting private ownership and civil order yet not stifled by any excessive legislation or taxation.

The good news is that that which worked in the past, will work in the future, and what didn’t work in the past will not work in the future either.

Sunday, September 4, 2011

Milk and 40 Countries Study

An old paper: "Differences in Coronary Mortality Can Be Explained by Differences in Cholesterol and Saturated Fat Intakes in 40 Countries but Not in France and Finland"

The study found that "...with comparable intakes of dietary cholesterol in France and Finland, the CHD mortality rate for men aged 55 to 59 was four times higher in Finland than in France."

In science, finding an exception to a theory always serves as an opportunity to revaluate the theory. Except with the "Fat And Cholesterol Theory" (of heart disease). Since Fat And Cholesterol Theory is treated as fact, finding exceptions to the theory has been used instead to revaluate the exceptions rather than the theory.

One reason that I would consider table 3 having higher chance of reflecting some possible real effects, is that it shows the countries of the similar culture, level of development and standard of living, where as the statistical correlations shown in table 1 are done over vastly dissimilar populations whose different level of development produces totally different set of health hazards that may completely mask any food influence.  For example, most developed countries exhibit both high meat consumption and high CHD (but also higher longevity!). Similar statistics done within one country show typically completely different correlation, the most striking feature is typically a disapearance of correlation between Coronary Heart Disease (CHD) and fat, like for example in Malmo Study.

Correlations between Cholesterol and Saturated (fat) Index (CSI) or other consumption attributes and heart disease across Europe may or may not reflect causal connections. There may be many spurious factors possibly involved. However, if we assume, for the sake of discussion that the correlations in Table 3 may be reflecting some causal connections, then this presents us immediately with another "paradox" and not just about France but also involving other West European countries! Namely, that cholesterol and saturated fat cannot possibly explain the huge discrepancy of CHD stats between France, Germany (West), UK and Finland! One immediately notices that while CHD almost doubles from one country to the next in table 3, cholesterol and saturated fat consumption index is roughly the same! More specifically, the fact that butterfat remains also roughly the same (given typical low accuracy of the food statistics) - automatically invalidates the authors' conclusion published at the end (at least the part implicating "butterfat"). Comparison of other factors (except milk) between Germany and the UK also shows no clear trend, yet the CHD is vastly different!

Milk on the other hand, shows a clearly rising consumption trend in Table 3, that tracks the magnitude of the CHD! Not milk fat, not butter and not milk protein (cheese) - just milk! Why milk, what milk, is it real or spurious? If real, does it apply only to milk in Europe or in other parts of the world as well?

Tuesday, August 30, 2011

Highest chocolate consumption = 37% reduction of CVD


Molten chocolate and a piece of a chocolate bar (Wiki)

New meta study:

Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis


From 4576 references seven studies met the inclusion criteria (including 114 009 participants). None of the studies was a randomised trial, six were cohort studies, and one a cross sectional study. Large variation was observed between these seven studies for measurement of chocolate consumption, methods, and outcomes evaluated. Five of the seven studies reported a beneficial association between higher levels of chocolate consumption and the risk of cardiometabolic disorders. The highest levels of chocolate consumption were associated with a 37% reduction in cardiovascular disease (relative risk 0.63 (95% confidence interval 0.44 to 0.90)) and a 29% reduction in stroke compared with the lowest levels.

Based on observational evidence, levels of chocolate consumption seem to be associated with a substantial reduction in the risk of cardiometabolic disorders. ...

(Click to open large jpg)

A few questions to ponder:

- Is it a real effect or are we witnessing a coincidental correlation, for example the "wealth" effect?

- If real, which factor contributed the most? One can think of several possible such as (a) cardiovascular-protective effects of coconut and cocoa butter, (b) resveratrol, (c) substitution of more harmful snacks and drinks (soda, beer etc), or some other yet unknown factor present in chocolate?

- What is the consumption quantity or threshold to produce a given effect.  (The study did not have the means to quantify chocolate consumption in physical units, due to the lack of published data).

- Since the cardioprotective effect is comparable if not higher than the hugely popular statin drugs (according to the mainstream but questionable studies), it would be interesting to notice how eagerly will medical science community rush to conduct more studies on this topic.  I am not holding my breath.

Added 15-Sep-2011

Chocolate 'as good for you as exercise'


Tuesday, August 16, 2011

Fat disrupts sugar sensors in pancreas causing type 2 diabetes


That's why a diet simultanously high in fat and carbs is detrimental, but a diet high in either one and not both, is not!

See on BBC health:

(Source: "Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport")

This is important finding that clears a lot of confusion. I used to answer countless of questions from diabetics (on other forums), the most frequent was this, paraphrasing:

"Why should I eat high fat diet if we know that it would increase my already high insulin resistance?"

This article is telling us that the answer to this is that it won't!

It will make pancreas stop reacting to blood glucose while you are eating fat AND carbohydrates at the same time. This won't matter you eat fat on its own with very little or no carbs! On the other hand, diabetic insulin resistance appears in this light to be a totally different phenomenon - related to body tissues and organs being permanently resistant to insulin that is already produced by pancreas and circulating throughout the body!

Will fat affect the tissue insulin resistance as well? Yes - probably by reducing it!  As me and millions of other people who tried Dr. Jan Kwasniewski's Optimal Diet, have found!

We are probably dealing here with two opposing effects:

1) Detrimental effect of dietary fat upon pancreas preventing it from reacting to blood glucose
(Which matters if and only if one consumes significant amount of carbohydrates together and simultaneously with fat).

2) Positive long term effect of dietary fat upon body tissues and organs

Can a fatty meal impair cardiovascular health? Absolutely, since it can lead to hyperglycemia due to (1) if the meal is also high in carbs  (I will pass that carrot cake, thank you...)

Can a high fat meal reduce the risk of cardiovascular disease (see this)? Absolutely! If it is low in carbohydrates!

This clarifies also another issue, namely Dr. Kwasniewski's claim that a diet with 35-45% fat by calories is the most detrimental to one's health (for adults). It makes a lot more sense in the light of this article. (Note: since a diet typically would contain 10-20% protein, therefore 35-45% fat means 35-55% carbohydrates, by calories).

Bottom line:
- Do not mix high carbohydrate diet with high fat nutrition!

------------ Update 30-Aug-2011 -------------------

Read this:

Fat and Diabetes: Bad Press, Good Paper, and the Reemergence of Our Good Friend Glutathione


Saturday, August 6, 2011

Warning MS C++ 2010 runtime upgrade breaks ATI graphics drivers! (off-topic)

I appologise for this quick off-topic warning post, but this info might save many of you from throwing out a perfectly good ATI Radeon 4xxx series that suddenly stopped working.  I use ATI HD4670 in Win7 32bit, but this may apply also to other series of ATI cards.

A very recent upgrade of Microsoft C++ run-time library version 2011.0.30xx to 2011.0.40xx (Win7 32bit) breaks ATI Radeon graphics drivers. The symptoms are similar to when a graphic card breaks due to a hardware failure, that is screen goes suddenly black during a boot up, in high resolution large screen mode, while it may still be working when booted in the "safe mode".

I haven't tracked down yet where that .40 upgrade came from but I have determined it by multiple trial and errors beyond reasonable doubt that it is caused by the Windows 7 system run-time library incompatibility.

To fix the problem:

1) If your screen is already black, shut down, remove ATI Radeon graphics card, plug in some other card (Nvidia or something much older, even a standard VGA will do). Reboot.

2) Open Control Panel, Programs and Features - Check if you have MS C++ 2010.0.40xx Run-time installed. If yes then uninstall it.

3) Go to go to ATI Radeon downloads section, download and install "ATI Catalyst Center" (this will install all necessary graphics drivers for the ATI Radeon series) . I installed an older version (10.12) but the most recent one (11.7) should also work They all install MS C++ 2010.0.30 run-time library, as part of their overall installation process - verify the log that it was installed OK! If you forgot to uninstall version 40 then this step of "ATI Catalyst" installation will report a failure!

4) Shut down the PC, remove the old graphics card, reinstall ATI Radeon, restart.

Saturday, July 23, 2011

Animal protein and osteoporosis myth


This is a compilation of my past discussions (2007). Since this issue comes back so often, I decided to re-post it here, as the reference [or just to annoy] 8-:) . 


Myth 1: "Populations which consume a very high amount of dairy get more hip fractures than those which don't."


Myth 2: "It isn't only the calcium that comes in which is important but the calcium which is leached out due to high animal protein diets.

I am sorry to disappoint the true believers, but it is just the opposite! People who avoid animal protein believing that they are saving their bones are in fact increasing the risk of osteoporosis.

The following study found that women who consumed the most animal protein (+43%) had only one-fifth risk of hip fractures:

"Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women"
by Ronald G Munger, James R Cerhan, and Brian C-H Chiu Am J Clin Nutr 1999;69:147-52.

Results: Forty-four cases of incident hip fractures were included in the analyses of 104 338 person-years (the number of subjects studied times the number of years of follow-up) of follow-up data. The risk of hip fracture was not related to intake of calcium or vitamin D, but was negatively associated with total protein intake. Animal rather than vegetable sources of protein appeared to account for this association. In a multivariate model with inclusion of age, body size, parity, smoking, alcohol intake, estrogen use, and physical activity, the relative risks of hip fracture decreased across increasing quartiles of intake of animal protein as follows: 1.00 (reference), 0.59 (95% CI: 0.26, 1.34), 0.63 (0.28, 1.42), and 0.31 (0.10, 0.93); P for trend = 0.037.

Conclusion: Intake of dietary protein, especially from animal sources, may be associated with a reduced incidence of hip fractures in postmenopausal women.

Table 4 of the study shows some really interesting data on the risk of hip fractures (from 6-th column). Namely, in addition to much lower (factor of 0.31) risk for the 43% higher consumption of animal protein, they found 1.9 times HIGHER risk associated with the 31% higher consumption of VEGETABLE protein!

Carbohydrate consumption turned out to have been a much bigger factor, perhaps the biggest factor:

23% higher consumption of carbohydrates was associated with 3 times higher rate of fractures!

If we recalculate (normalize) those risk factors per 100% (i.e. per doubling) increase of the consumption of each: total protein, animal protein, veg protein and carbohydrates, then we obtain the following:

Hip fracture risk correlation:

  • Total protein: - risk reduction 3.6 times
  • Animal protein:- risk reduction 4.5 times
  • Vegetable protein:- risk INCREASE 2.9 times
  • Carbohydrate:- risk INCREASE 4.9 times

In addition, women who experienced hip fractures (as opposed to those who didn't) consumed less animal fat, less saturated fat, less alcohol, had lower body mass index, had fewer pregnancies, smoked less, consumed more calcium, more vegetable fat and more vit D.




"Controlled High Meat Diets Do Not Affect Calcium Retention or Indices of Bone Status in Healthy Postmenopausal Women"

"Protein intake: effects on bone mineral density and the rate of bone loss in elderly women"

"Effect of Dietary Protein on Bone Loss in Elderly Men and Women: The Framingham Osteoporosis Study"

"Factors associated with calcium absorption efficiency in pre- and perimenopausal women"

Quote: "Women in the lowest tertile of the ratio of dietary fat to fiber had 19% lower fractional calcium absorption values than did women in the highest tertile of ratio of dietary fat to fiber"


"Protein Saves Bone in Elders"

"New Data on Dietary Protein and Bone"

------ More references, update 1-Aug-2001 ---------------------------------------

This is based on the most recent blog article by Denise Minger quoting various peer-reviewed publications using China Study data. This is a MUST READ!

Some of the papers were co-authored by the well known expert vegan scientist Dr. T.Colin Campbell but unlike in his popular book, those papers are based on individual rather than county-averaged data. They also state completely opposite conclusion regarding heart disease, cancer and bone health which is quite remarkable for a senior mainstream academic scientist! The same man but two opposite views! Now to the subject of osteoporosis, bone density, calcium and diet:

* Dietary calcium and bone density among middle-aged and elderly women in China" by Ji-Fan Hu, Xi-He Zhao, Jian-Bin Jia, Banoo Parpia, and T. Colin Campbell.

However, decline in bone mass after menopause for women in county WA (higher dairy calcium) was at a somewhat slower rate than for women in the nonpastoral areas (without dairy calcium).

Thus. differences in the rate of bone loss between these areas may be related to differences in dairy calcium intake, given that 34.6% ofealcium in county WA and none in the other nonpastoral areas was from milk. Indeed, dairy calcium was found to be more significantly correlated with bone mass than was nondairy calcium (Table 7), even though these analyses only included women with dairy food intake in counties YA and WA (n= 253). Nondairy calcium. in contrast, showed no association with bone variables after age and/or body weight were adjusted for (Table 7).

BMC and BMD at the distal and midradius were positively associated with consumption of milk (r = 0. 1 5-0.26, P [less than] 0.003) and with consumption of hard cheese and other dairy foods (r = 0.22-0.29, P [less than] 0.01) (data not shown). These results agree with those reported in other cross-sectional studies (35, 37). A similar association between daily milk intake and bone density was also reported by Yano et al (10) in Hawaiian Japanese males and females and by Shiehita (23) in 85 healthy Japanese males and females, whose calcium intakes were as low as in our study. Increasing calcium intake with calcium-rich foods (milk and cheese) was found to reduce bone loss in adolescent (34), osteoporotic (38), premenopausal (14), and lactating (39) women.

* Veganism and osteoporosis: A review of the current literature. "The findings gathered consistently support the hypothesis that vegans do have lower bone mineral density than their non-vegan counterparts."

* A Comparison of Bone Mass Measurements of Vegetarians and Omnivores. "In this review of 9 cross-sectional and 1 longitudinal study, little statistical significance between bone density and bone content was found between vegetarians and omnivores."

* Effect of vegetarian diets on bone mineral density: a Bayesian meta-analysis. "The results suggest that vegetarian diets, particularly vegan diets, are associated with lower BMD, but the magnitude of the association is clinically insignificant."

* Long-Term Vegetarian Diet and Bone Mineral Density in Postmenopausal Taiwanese Women. "Long-term practitioners of vegan vegetarian were found to be at a higher risk of exceeding lumbar spine fracture threshold … and of being classified as having osteopenia of the femoral neck."

The rest of Denise article quotes more papers co-authored by T.C.Campbell, that conclude a positive protective role of dairy, meat and fish rich diets against cancer, heart disease and other disease in China. Read it all!


Saturday, July 9, 2011

Vegans, dietary fat and Alzheimer's

I like browsing through some vegan discussion groups looking at the papers, publications and studies they use to support their belief system. McDougall's forum is particularly useful because of their tenacity in trying to use science to justify themselves. Experience taught me that such studies are always ambivalent and very often prove a completely opposite views to those of the vegan believers who posted them.

The following study from 2003, did not disappoint me:

Dietary fats and the risk of incident Alzheimer disease.

The abstract looked very foreboding, for example, quote:
Persons in the upper fifth of saturated-fat intake had 2.2 times the risk of incident Alzheimer disease compared with persons in the lowest fifth

Not all is lost fortunately, because of the widely known practice in the medical "science" to print only the politically correct (i.e. false) information in the abstracts while hiding the true albeit inconvenient facts in the full text.

The facts are that the saturated fat data and most of the other results are generally not statistically significant!

The facts are that even when one takes the trend line across saturated fat quintiles and makes it appear statistically more significant than an individual datum (the so-called "p value for the trend") - the resulting p is still much greater than 0.05 and thus is still not statistically significant! Best illustration is the following (upper) portion of the Table 3:

The facts are that if you take the most basic age-adjusted only data (look at the first row called "Age-adjusted+"), there is no clear trend at all since the middle and the second highest saturated fat columns (quintiles) have exactly the same Alzheimer's risk as the lowest reference quintile of saturated fat!  The second and the third row (headed by "Multivariable" and "Multivariable... other fats") above are the more processed data, that seem to exhibit a weak rising trend, albeit also not statistically significant!  One shall always keep in mind that multivariable-corrected trends are dependent upon some specific model-dependent assumptions that may or may not be correct.

It gets more intereseting as one reads down the table. If one takes the above discussed saturated results on faith, beliving that the weak statistics may be reflecting some real underlying trend rather than being some artefacts of the data gathering and processing methodology (as I suspect is the case), then one should also take a notice and state that the rest of the data "proves" (also not statistically significanly) that the total fat consumption, dietary cholesterol intake, animal fat consumption and vegetable fat consumption all seem either not to correlate or to correlate NEGATIVELY (protectively) with the Alzheimer's risk! See the lower portion of the Table 3:

For example, the total fat consumption seems to be protective against Alzheimer's! The second lowest and the middle quintile in consumption of animal produce (indicated by dietary cholesterol!) also have higher Alzheimer's risk than the two highest quintiles! Animal fat consumption seems to show no correlation to Alzheimer - the trend curve is pretty flat except the third row ("Multivariable adjusted for vegetable fats and trans-fats") which shows a weak NEGATIVE (i.e. protective) trend!

Last but not least the bottom group Vegetable fats shows the strongest correlation in the whole study. That correlation is strongly NEGATIVE (protective), that is the more vegatable fat the less Alzheimer's cases! In fact that result, after "Multivariable adjusted for vegetable fats and trans-fats" - is the only one, alongside the omega-6 fat result ( which is basically its subset) that does exhibit a statistically significant trend!

Unfortunately for those who believe in the low fat dogma, this is not a good news! Especially when compared with other sources, see for example this and that.

Thursday, July 7, 2011

Do statins or low fat diets cause osteoporosis?

New study: "Association Between Myocardial Infarction and Fractures: An Emerging Phenomenon."

Most interesting is this, quote:

...substantial temporal variations were noted (
1979 to 1989: hazard ratio, 0.81 ...
1990 to 1999: hazard ratio, 1.47 ...
2000 to 2006: hazard ratio, 1.73 ...
Trends were similar regardless of age, sex or fracture site. Conversely, the overall hazard ratio for death in MI cases versus controls did not change materially...

The only obvious factor that was different in the first decade (blue - less osteoporosis following a MI event) as opposed to the second and third decade of the study (red - more osteoporosis!) is the common usage of statin drugs! Perhaps a popularity of the low fat high carbohydrate diets in treating MI patients (the so-called AHA diet) may be another factor distinguishing the red from the blue decades.


Update 16-July-2011

Another recent study found on Dr.McDougall forum, linking bone underdevelopment with malnutrition, in this case a lack of dairy products:

Thin Bones Seen In Boys with Autism and Autism Spectrum Disorder

The boys in the study who were on a casein-free [READ DAIRY-FREE (added by H.)] diet had the thinnest bones. In fact, the 9 boys who were on a casein-free diet had bones that were 20 percent thinner than normal for children their age. Boys who were not on a casein-free diet showed a 10 percent decrease in bone thickness when compared to boys with normal bone development.

The study authors wrote that bone development of children on casein-free diets should be monitored very carefully. They noted that studies of casein-free diets had not proven the diets to be effective in treating the symptoms of autism or ASD.

As a side note from my own experience. It reminds me that a nurse examining children at my school in the Eastern Europe, 1960-ties (I was around 12) told us that many, about a half had unusually thin but long bones in their hands and different elbow joints, as compared with the medical reference books that she used. Those children had normal food intake, were rather well fed. I always wondered what was causing the difference and that the same factor affecting bone development may have also affected the risk of autism! What was that factor? We didn't eat breakfast cereals nor drank pop. We ate a high carb medium fat diet not much different from that of the 1930-ties or before. Definitely more sugar - sugar became very cheap in the 1960-ties, and margarine became the new "health" "food" of the day plus vegetable oils became a popular cooking fat substitute in the 1970-ties. Sugar was very expensive before WWII in Poland due to special sugar tax, then became completely unavailable during German occupation 1939-1945 and then became cheap afterwards. What else other than sugar could have done the damage?


Sunday, July 3, 2011

The end of an era

Drawn by Cecilia Bleszynski

The following Washington Post article "Final NASA shuttle mission clouded by rancor" should have had a different headline. Imagine this:


Saturday, July 2, 2011

Vitamin K2 Reduces Heart Disease by 57 Percent

Interesting links, some new some old. Enjoy!

From Natural Health Digest and News

Researchers concluded that vitamin K1 had little effect on cardiovacular health, but vitamin K2 dramatically reduced it.
How do you get vitamin K2 into your diet? Vitamin K2 is found largely in meats and eggs.

Also cheese, organ meat, natto. See also my old posts on vitamin K2 related topics

Other interesting links gathered from a vegan forum (thank you Dr. Mc Dougall):

Sci Am: "Carbs against Cardio..." (refresher of an older post)

"Saturated Fat and Cholesterol Do Not Cause Coronary Heart Disease" by Dr. Paul J. Rosch


4. No association between cholesterol levels and the severity or extent of atherosclerosis has ever been found in postmortem studies of the general population. No clinical or imaging study has found any relation between the degree of cholesterol lowering and improvement.

In one angiography study, in which blood cholesterol had been reduced by more than 25% in 24 patients, atherosclerosis was increased in 18 and unchanged in eight. Cholesterol rose in 12 other patients but only 4 showed an increase in atherosclerosis. A Mayo Clinic study similarly found that in all patients whose cholesterols had decreased by more than 60, there was a significant increase in coronary atherosclerosis.
6. The huge and lengthy MRFIT study (Multiple Risk Factor Intervention Trial) was designed to prove the links between diet, cholesterol, and other Framingham risk factors with heart disease. Cholesterol consumption was cut by 42 percent, and saturated fat consumption by 28 percent and on long-term follow-up, those adhering to this dietary fat restriction had slightly lower coronary heart disease death rates.

However, this benefit was far outweighed by significantly increased total mortality rates, especially from hemorrhagic stroke, cancer, suicide, accidents and violence. The risk of dying from a cerebral hemorrhage was 500% greater in those with low cholesterol compared to those with high levels. In most other studies, the incidence of stroke was higher in those who ate less saturated fat.