Malocclusion: Disease of Civilization

In his epic work Nutrition and Physical Degeneration, Dr. Weston Price documented the abnormal dental development and susceptibility to tooth decay that accompanied the adoption of modern foods in a number of different cultures throughout the world. Although he quantified changes in cavity prevalence (sometimes finding increases as large as 1,000-fold), all we have are Price's anecdotes describing the crooked teeth, narrow arches and "dished" faces these cultures developed as they modernized.

Price published the first edition of his book in 1939. Fortunately, Nutrition and Physical Degeneration wasn't the last word on the matter. Anthropologists and archaeologists have been extending Price's findings throughout the 20th century. My favorite is Dr. Robert S. Corruccini, currently a professor of anthropology at Southern Illinois University. He published a landmark paper in 1984 titled "An Epidemiologic Transition in Dental Occlusion in World Populations" that will be our starting point for a discussion of how diet and lifestyle factors affect the development of the teeth, skull and jaw (Am J. Orthod. 86(5):419)*.

First, some background. The word occlusion refers to the manner in which the top and bottom sets of teeth come together, determined in part by the alignment between the upper jaw (maxilla) and lower jaw (mandible). There are three general categories:

• Class I occlusion: considered "ideal". The bottom incisors (front teeth) fit just behind the top incisors.
• Class II occlusion: "overbite." The bottom incisors are too far behind the top incisors. The mandible may appear small.
  
• Class III occlusion: "underbite." The bottom incisors are beyond the top incisors. The mandible protrudes.
  

Malocclusion means the teeth do not come together in a way that's considered ideal. The term "class I malocclusion" is sometimes used to describe crowded incisors when the jaws are aligning properly.

Over the course of the next several posts, I'll give an overview of the extensive literature showing that hunter-gatherers past and present have excellent occlusion, subsistence agriculturalists generally have good occlusion, and the adoption of modern foodways directly causes the crooked teeth, narrow arches and/or crowded third molars (wisdom teeth) that affect the majority of people in industrialized nations. I believe this process also affects the development of the rest of the skull, including the face and sinuses.

In his 1984 paper, Dr. Corruccini reviewed data from a number of cultures whose occlusion has been studied in detail. Most of these cultures were observed by Dr. Corruccini personally. He compared two sets of cultures: those that adhere to a traditional style of life and those that have adopted industrial foodways. For several of the cultures he studied, he compared it to another that was genetically similar. For example, the older generation of Pima indians vs. the younger generation, and rural vs. urban Punjabis. He also included data from archaeological sites and nonhuman primates. Wild animals, including nonhuman primates, almost invariably show perfect occlusion.

The last graph in the paper is the most telling. He compiled all the occlusion data into a single number called the "treatment priority index" (TPI). This is a number that represents the overall need for orthodontic treatment. A TPI of 4 or greater indicates malocclusion (the cutoff point is subjective and depends somewhat on aesthetic considerations). Here's the graph: Every single urban/industrial culture has an average TPI of greater than 4, while all the non-industrial or less industrial cultures have an average TPI below 4. This means that in industrial cultures, the average person requires orthodontic treatment to achieve good occlusion, whereas most people in more traditionally-living cultures naturally have good occlusion.

The best occlusion was in the New Britain sample, a precontact Melanesian hunter-gatherer group studied from archaeological remains. The next best occlusion was in the Libben and Dickson groups, who were early Native American agriculturalists. The Pima represent the older generation of Native Americans that was raised on a somewhat traditional agricultural diet, vs. the younger generation raised on processed reservation foods. The Chinese samples are immigrants and their descendants in Liverpool. The Punjabis represent urban vs. rural youths in Northern India. The Kentucky samples represent a traditionally-living Appalachian community, older generation vs. processed food-eating offspring. The "early black" and "black youths" samples represent older and younger generations of African-Americans in the Cleveland and St. Louis area. The "white parents/youths" sample represents different generations of American Caucasians.

The point is clear: there's something about industrialization that causes malocclusion. It's not genetic; it's a result of changes in diet and/or lifestyle. A "disease of civilization". I use that phrase loosely, because malocclusion isn't really a disease, and some cultures that qualify as civilizations retain traditional foodways and relatively good teeth. Nevertheless, it's a time-honored phrase that encompasses the wide array of health problems that occur when humans stray too far from their ecological niche. I'm going to let Dr. Corruccini wrap this post up for me:

I assert that these results serve to modify two widespread generalizations: that imperfect occlusion is not necessarily abnormal, and that prevalence of malocclusion is genetically controlled so that preventive therapy in the strict sense is not possible. Cross-cultural data dispel the notion that considerable occlusal variation [malocclusion] is inevitable or normal. Rather, it is an aberrancy of modern urbanized populations. Furthermore, the transition from predominantly good to predominantly bad occlusion repeatedly occurs within one or two generations' time in these (and other) populations, weakening arguments that explain high malocclusion prevalence genetically.

* This paper is worth reading if you get the chance. It should have been a seminal paper in the field of preventive orthodontics, which could have largely replaced conventional orthodontics by now. Dr. Corruccini is the clearest thinker on this subject I've encountered so far.

Diabetics on a Low-carbohydrate Diet, Part II

I just found another very interesting study performed in Japan by Dr. Hajime Haimoto and colleagues (free full text). They took severe diabetics with an HbA1c of 10.9% and put them on a low-carbohydrate diet:

The main principle of the CRD [carbohydrate-restricted diet] was to eliminate carbohydrate-rich food twice a day at breakfast and dinner, or eliminate it three times a day at breakfast, lunch and dinner... There were no other restrictions. Patients on the CRD were permitted to eat as much protein and fat as they wanted, including saturated fat.

What happened to their blood lipids after eating all that fat for 6 months, and increasing their saturated fat intake to that of the average American? LDL decreased and HDL increased, both statistically significant. Oops. But that's water under the bridge. What we really care about here is glucose control. The patients' HbA1c (glycated hemoglobin; a measure of average blood glucose over the past several weeks) declined from 10.9 to 7.4%.

Here's a graph showing the improvement in HbA1c. Each line represents one individual:

Every single patient improved, except the "dropout" who stopped following the diet advice after 3 months (the one line that shoots back up at 6 months). And now, an inspirational anecdote from the paper:

One female patient had an increased physical activity level during the study period in spite of our instructions. However, her increase in physical activity was no more than one hour of walking per day, four days a week. She had implemented an 11% carbohydrate diet without any antidiabetic drug, and her HbA1c level decreased from 14.4% at baseline to 6.1% after 3 months and had been maintained at 5.5% after 6 months.

That patient began with the highest HbA1c and ended with the lowest. Complete glucose control using only diet and exercise. It may not work for everyone, but it's effective in some cases. The study's conclusion:

...the 30%-carbohydrate diet over 6 months led to a remarkable reduction in HbA1c levels, even among outpatients with severe type 2 diabetes, without any insulin therapy, hospital care or increase in sulfonylureas. The effectiveness of the diet may be comparable to that of insulin therapy.

Diabetics on a Low-carbohydrate Diet
The Tokelau Island Migrant Study: Diabetes

UNUSUAL REMEDIES

Pfaffia ( Amaranthaceae ). This herb is grown in Central and Southern America and is known as Brazilian Ginseng. The roots have been used by natives as a cure all, but more widely as a tonic aphrodisiac.


Pfaffia has been used internally for stress, chronic fatigue,debility, poor appetite, Epstein-Barr disease, glandular fever, infertility, impotence, menstrual and menopausal problems, diabetes, pancreas dysfunctions, ulcers, rheumatism, hypertension, cardiovascular disease, nervous disorders, chronic degenerative disease, and various kinds of cancer. Also to improve resistance to infection and increase stamina.


Extracts are added to food supplements and herbal tonics.

Another Fatty Liver Reversal, Part II

A month ago, I wrote about a reader "Steve" who reversed his fatty liver using a change in diet. Non-alcoholic fatty liver disease (NAFLD) is a truly disturbing modern epidemic, rare a few decades ago and now affecting roughly a quarter of the adult population of modern industrialized nations. Researchers cause NAFLD readily in rodents by feeding them industrial vegetable oils or large amounts of sugar.

Steve recently e-mailed me to update me on his condition. He also passed along his liver test results, which I've graphed below. ALT is a liver enzyme that enters the bloodstream following liver damage such as hepatitis or NAFLD. It's below 50 units/L in a healthy person*. AST is another liver enzyme that's below 35 units/L in a healthy person*.

Steve began his new diet in November of 2008 and saw a remarkable and sustained improvement in his ALT and AST levels:

Here's how Steve described his diet change to me:

I totally eliminated sugar, heavy starches, and grains. Started eating more whole, real foods, including things like grass-fed beef and pastured pork and eggs, began supplementing with good fats and omega-3 (pastured butter, coconut oil, cod liver oil). Ate more fruits and vegetables instead of refined carbs. Also completely gave up on the idea that I had to eat only "lean" meats. After my last results, the GI doc said that I wouldn't need the biopsy at all, that things were great, and that if I kept it up I "would live forever."

He did experience some side effects from this diet though:

My triglycerides also went from pre-diet measures of 201 and 147 to post diet 86, 81, and 71.

The added bonus, of course, was that my weight went from 205 pounds to 162 pounds and my body fat percentage from 24% to 12% in the matter of five months--all without the typically excessive cardio I used to try unsuccessfully for weight loss.

The liver is the body's "metabolic grand central station". It's essential for nutrient homeostasis, insulin sensitivity, detoxification, and hormone conversion, among other things. What's bad for the liver is bad for the rest of the body as well. Don't poison your liver with sugar and industrial vegetable oils.


* The cutoff depends on who you ask, but these numbers are commonly used.

How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
Fatty Liver Reversal
Another Fatty Liver Reversal

Human Growth Hormone Supplements - The Facts

By Bethany Jordin

HGH supplements are one of the latest craze today in the
field of health and supplementation. With all the talk about
HGH supplements, let us discuss the facts and separate them
from the fiction that's been going around about HGH products
in the market.

There are of course literally hundreds of websites marketing
and selling HGH supplements. It is a huge niche market. As
you would expect, every company claims to have the best
product that out-performs all of the others. But is it true?

So how to sort out the jokers from the good guys; the good
product from the bad; those that really do work, from those
that really don't? There are some crooks out there who will
sell you a harmless but ineffective placebo because they
make more profit that way. But how can you recognize and
avoid them? One way of spotting the rogues is by the
exaggerated claims that they make about their product. So
let's have a look at a few of these wild claims and see if
any of them hold any water.

Claim: That HGH supplements add up to 8.8% of genuine extra
muscle tone, and that you will also lose 14.4% of your body
fat without having to do any physical exercise or having to
go on a calorie controlled diet. Our response: The figures
used in this claim are taken from research done by Dr Rudman
in 1990. Whilst the figures themselves are true, his
methodology was to use injections of HGH. The supplemental
product making this claim is in capsule format. Capsules
deliver a significantly smaller dose of HGH than do
injections, and therefore any comparison is invalid.
Capsules can, and do work, but it is over a longer duration,
by slow build up.

Claim: Our pill/powder/spray contains the real human growth
hormone. Fact: First, know that HGH is a prescription drug.
If you put real HGH in significant amounts, it will no
longer be considered a supplement, but a drug. A drug can
only be sold with prescription, so technically it is illegal
to market them without it. Most websites market HGH
supplements that either contain homeopathic amounts of HGH -
meaning really minute amounts (up to 2 micrograms), or HGH
boosters/releasers which contain ingredients that stimulate
the natural production of HGH in the brain.

Claim: The FDA approves the HGH used in their product. Our
response: This is incorrect. The FDA does not get involved
in any way, shape, or form, with the health food supplement
industry, of which HGH supplements are a part. This lack of
regulation is one of the reasons that there are so many
different supplemental products on the market, but in truth,
none of them can be FDA approved. If they say they are, they
lie.

So are there supplements worth taking? Although this article
outlines some of the points to be careful about when buying
HGH supplements, it does not deny the fact that many HGH
products sold by reliable websites are actually effective.
It is only a matter of choosing the right website to trust,
and staying away from sellers who make false claims just to
make a sale.

HGH supplements are worth taking if you choose the right
brand and company to buy from. As with all supplements it is
advisable to consult your professional health care provider
before adding HGH supplements to your lifestyle.

Bethany Jordin is an Information Technology professional and
aspiring writer who focuses on topics relating to herbal
supplementation. For more on the benefits and safety of
(http://www.best-hgh-releasers.com/hgh-supplements.html) HGH
supplements visit (http://www.best-hgh-releasers.com)

TOP THREE NATURAL HEALERS.

I did some research into herbal healing and found the top three natural healers can all be grown in your garden. They are used in alternative health as healers for a number of conditions.

1. Chamomile. The flowers from chamomile can be used in a tea and are calming and soothing and especially beneficial to the nerves and digestion. It is also very good for skin irritaions.

2. Rosemary. Rosemary helps memory and concentration, improves mood and sweetens breath.

3. Lavender. This herb can calm and relax, eases pain, and is an antiseptic for cuts and bruises.

I have grown all three herbs in my garden and use them on myself and family for all the above medicinal reasons.

Do you need help?

Do you need help with a health related problem?. Can I help with an alternative health remedy?. I am not a qualified person in relation to holistic cures but I do however have a wealth of information on this subject, and my aim is to help people who have any illness or disease

You can contact me here at Natural cures or at curesforyou on twitter

I look forward to hearing from you.

The very best of health to all of you.

Acupressure point to boost the immune system

Try this exercise every day, It strengthens the kidneys and the immune system, and boosts vitality.

The location of this acupressure point is on the lower back two finger widths on either side of the spine, approximately level with the waist. So that is in the centre of the back.

Fold your hands into the shape of a fist. Now bring your hands behind your back and using the knuckle of the hands use a rolling action around either side of the spine.

Try not to press too hard, do this for about one minute, once each day.

Diabetics on a Low-carbohydrate Diet

Diabetes is a disorder of glucose intolerance. What happens when a diabetic eats a low-carbohydrate diet? Here's a graph of blood glucose over a 24 hour period, in type II diabetics on their usual diet (blue and grey triangles), and after 5 weeks on a 55% carbohydrate (yellow circles) or 20% carbohydrate (blue circles) diet:


The study in question describes these volunteers as having "mild, untreated diabetes." If 270 mg/dL of blood glucose is mild diabetes, I'd hate to see severe diabetes! In any case, the low-carbohydrate, high-fat diet brought blood glucose down to an acceptable level without requiring medication.

It's interesting to note in the graph above that fasting blood glucose (18-24 hours) also fell dramatically. This probably reflects improved insulin sensitivity in the liver. The liver pumps glucose into the bloodstream when it's necessary, and insulin suppresses this. When the liver is insulin resistant, it doesn't respond to the normal signal that there's already sufficient glucose, so it releases more and increases fasting blood glucose. When other tissues are insulin resistant, they don't take up the extra glucose, also contributing to the problem.

Glycated hemoglobin (HbA1c), a measure of average blood glucose concentration over the preceding few weeks, also reflected a profound improvement in blood glucose levels in the low-carbohydrate group:

At 5 weeks, the low-carbohydrate group was still improving and headed toward normal HbA1c, while the high-carbohydrate group remained at a dangerously high level. Total cholesterol, LDL and HDL remained unchanged in both groups, while triglycerides fell dramatically in the low-carbohydrate group.

When glucose is poison, it's better to eat fat.

Graph #1 was reproduced from Volek et al. (2005), which re-plotted data from Gannon et al. (2004). Graph #2 was drawn directly from Gannon et al.

Do you smoke?

I don't smoke myself but I do chew nicotine gum and I don't know why I started. I intend to look at alternative health ways of replacing the gum, perhaps with some natural remedy.

I don't have anything against smokers, my dad smoked cigarettes and then a pipe, although he did die quite young, at 64 from lung disease.

What I would like to know is would you be prepared to stop if you could find a way to stop the craving?.

Do you want to stop?.
Do you know of any alternative ways to stop smoking?.
I would be very interested to know. Please add your comments.
Thank you.

Free Blog Promotion - Blog and Blog resource Directory







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Ear Adrenal Acupoint helps craving for smoking.

By using this Acupressure point this is a simple, natural way to stimulate the adrenal gland and thus helps to remove cigarette craving.

Use your thumb and forfinger to locate the top of the ear, on the border of the indentation. Gently stimulate the point for about sixty seconds on each ear. This should be done each time you have a craving to smoke. Take care not to damage sensitive skin of the ear.

Natural Health Strategies

Necrotizing fasciitis: A deadly bug

A deadly bug called Necrotizing fasciitis: has killed a 54 year old man from Devon. The man had complained of a sore throat a week earlier, he was prescribed painkillers. He then developed pain in his left ankle less than 24 hours before he died. His condition deteriorated quickly until his family rushed him to the Royal Devon and Exeter Hospital at 3.10am. He was taken straight to theatre where surgeons tried to cut away the diseased tissue but the infection was spreading too quickly. He died a few hours later>

I am posting this blog as I am very concerned at the speed that this bug can kill, we need to know more information about it and what can be done to stop it. My heart goes out to this mans family and friends.
http://www.thesun.co.uk/sol/homepage/news/2624465/Flesh-eating-bug-kills-dad-in-four-hours.html

http://www.wrongdiagnosis.com/treat/penicillin.htm

Paleolithic Diet Clinical Trials Part IV

Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells.

After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.

Patients were put on two different diets for 3 months each. The first was a "conventional diabetes diet". I read a previous draft of the paper in which I believe they stated it was based on American Diabetes Association guidelines, but I can't find that statement in the final draft. In any case, here are the guidelines from the methods section:

The information on the Diabetes diet stated that it should aim at evenly distributed meals with increased intake of vegetables, root vegetables, dietary fiber, whole-grain bread and other whole-grain cereal products, fruits and berries, and decreased intake of total fat with more unsaturated fat. The majority of dietary energy should come from carbohydrates from foods naturally rich in carbohydrate and dietary fiber. The concepts of glycemic index and varied meals through meal planning by the Plate Model were explained [18]. Salt intake was recommended to be kept below 6 g per day.

The investigators gave the paleolithic group the following advice:

The information on the Paleolithic diet stated that it should be based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts, while excluding dairy products, cereal grains, beans, refined fats, sugar, candy, soft drinks, beer and extra addition of salt. The following items were recommended in limited amounts for the Paleolithic diet: eggs (≤2 per day), nuts (preferentially walnuts), dried fruit, potatoes (≤1 medium-sized per day), rapeseed or olive oil (≤1 tablespoon per day), wine (≤1 glass per day). The intake of other foods was not restricted and no advice was given with regard to proportions of food categories (e.g. animal versus plant foods). The evolutionary rationale for a Paleolithic diet and potential benefits were explained.

Neither diet was restricted in calories. After comparing the effects of the two diets for 3 months, the investigators concluded that the paleolithic diet:

• Reduced HbA1c more than the diabetes diet (a measure of average blood glucose)
• Reduced weight, BMI and waist circumference more than the diabetes diet
• Lowered blood pressure more than the diabetes diet
  
• Reduced triglycerides more than the diabetes diet
• Increased HDL more than the diabetes diet

However, the paleolithic diet was not a cure-all. At the end of the trial, 8 out of 13 patents still had diabetic blood glucose after an oral glucose tolerance test (OGTT). This is compared to 9 out of 13 for the diabetes diet. Still, 5 out of 13 with "normal" OGTT after the paleolithic diet isn't bad. The paleolithic diet also significantly reduced insulin resistance and increased glucose tolerance, although it didn't do so more than the diabetes diet.

As has been reported in other studies, paleolithic dieters ate fewer total calories than the comparison group. This is part of the reason why I believe that something in the modern diet causes hyperphagia, or excessive eating. According to the paleolithic diet studies, this food or combination of foods is neolithic, and probably resides in grains, refined sugar and/or dairy. I have my money on wheat and sugar, with a probable long-term contribution from industrial vegetable oils as well.

Were the improvements on the paleolithic diet simply due to calorie restriction? Maybe, but keep in mind that neither group was told to restrict its caloric intake. The reduction in caloric intake occurred naturally, despite the participants presumably eating to fullness. I suspect that the paleolithic diet reset the dieters' body fat set-point, after which fat began pouring out of their fat tissue. They were supplementing their diets with body fat-- 13 pounds (6 kg) of it over 3 months.

The other notable difference between the two diets, besides food types, was carbohydrate intake. The diabetes diet group ate 56% more carbohydrate than the paleo diet group, with 42% of their calories coming from it. The paleolithic group ate 32% carbohydrate. Could this have been the reason for the better outcome of the paleolithic group? I'd be surprised if it wasn't a factor. Advising a diabetic to eat a high-carbohydrate diet is like asking someone who's allergic to bee stings to fetch you some honey from your bee hive. Diabetes is a disorder of glucose intolerance. Starch is a glucose polymer.

Although to be fair, participants on the diabetes diet did improve in a number of ways. There's something to be said for eating whole foods.

This trial was actually a bit of a disappointment for me. I was hoping for a slam dunk, similar to Lindeberg's previous study that "cured" all 14 patients of glucose intolerance in 3 months. In the current study, the paleolithic diet left 8 out of 13 patients diabetic after 3 months. What was the difference? For one thing, the patients in this study had well-established diabetes with an average duration of 9 years. As Jenny Ruhl explains in her book Blood Sugar 101, type II diabetes often progresses to beta cell loss, after which the pancreas can no longer secrete an adequate amount of insulin.

This may be the critical finding of Dr. Lindeberg's two studies: type II diabetes can be prevented when it's caught at an early stage, such as pre-diabetes, whereas prolonged diabetes may cause damage that cannot be completely reversed though diet. I think this is consistent with the experience of many diabetics who have seen an improvement but not a cure from changes in diet. Please add any relevant experiences to the comments.

Collectively, the evidence from clinical trials on the "paleolithic diet" indicate that it's a very effective treatment for modern metabolic dysfunction, including excess body fat, insulin resistance and glucose intolerance. Another way of saying this is that the modern industrial diet causes metabolic dysfunction.

Paleolithic Diet Clinical Trials
Paleolithic Diet Clinical Trials Part II
One Last Thought
Paleolithic Diet Clinical Trials Part III

Exercise for your lungs

This exercise will help any type of lung problem, asthma, bronchitis, or breathing difficulties.

It strengthens the entire breathing system, including the skin, which is often called the " third lung".

To determine the health of the lungs and body, one should measure the length of the inhalation and exhalation. If the exhalation is longer than the inhalation, ill health is indicated, since more is going out of the lungs than is coming in.

1. Stand with your feet shoulder-width apart and parallel to each other. Your back should be straight, your chin slightly toward your chest, and your head erect, as if the back of your neck is stretching upward.

2. Exhale all the air from your lungs and clasp your hands behind your back.

3. Now inhale slowly, expanding your lungs and pushing your hands away from your back. Keep your chin tucked into your chest, and use only your chest to breathe.

4. Exhaling, drop your hands and bring your arms out in front of you. Continue to raise your arms, bringing your hands up toward your head and then around behind your back, and back up in front of your body, completing one cycle.

5. Interlace your fingers behind your back and begin the exercise again on the inhalation.

The cycle should be done ten times, and the exercise once per day.

Quit smoking tools : http://smokefree.nhs.uk/quit-tools/?WT.mc_id=search&gclid=CO2B9uXS6ZwCFYYU4wodIBm9jg

Prostate cancer could be linked with a virus

Scientists have identified a virus which they believe could trigger some cases of prostate cancer. Researchers hope that, if proven, the findings could lead to a test and possibly even a vaccine against the deadly form of cancer: http://www.telegraph.co.uk/health/healthnews/6151243/Virus-could-trigger-some-cases-of-prostate-cancer.html

The best natural way to stop Prostate cancer is by prevention. You can do this by using the mineral Magnesium and zinc. Magnesium is an important mineral it maintains strong bones and tooth enamel, calms the nervous system, regulates heartbeat, strengthens digestion but more importantly maintains a healthy prostate in men.

Lycopene which is found in tomatoes can also significantly reduce the risk of prostate cancer. It is available in capsule form as a nutritional supplement from health food shops.

The herb Saw Palmetto ( Serenoa Serrulata) has also anti-cancer benefits. The berries from the herb have been found to inhibit the hormonal secretion of the prostate and is therefore used as treatment for enlarged prostate.

Animal Models of Atherosclerosis: Diet-Induced Atherosclerosis

LDL likely plays a role in causing atherosclerosis, with the majority of the damage coming from the oxidized form of LDL. There are at least two ways to increase the concentration of oxidized LDL (oxLDL) in the blood: 1) increase the total concentration of LDL while keeping the proportion of oxLDL the same; 2) increase the proportion of oxLDL. Dietary fats differ in their effects on these two factors, and the net outcome is also dependent on the species eating the fat and the overall dietary context.

The omega-6 polyunsaturated fat, linoleic acid (LA; found abundantly in industrial vegetable oils), may be a factor in the susceptibility of LDL to oxidation. LDL is rich in LA regardless of diet, yet the amount of LA in LDL still depends on diet to a certain degree. Thus, on the surface, one would expect a diet high in industrial vegetable oil to promote atherosclerosis. Unfortunately, it's not that simple, because LA also lowers the amount of LDL in the blood of a number of species, including humans.

The amount of atherosclerosis produced by feeding different fats depends both on how much LDL oxidation occurs and on how the fat affects the organism's blood lipid profile. For example, if corn oil lowers LDL by 3-fold relative to lard in a rabbit model, yet increases the proportion of oxLDL by 50%, the rabbit will probably develop more atherosclerosis eating lard than eating corn oil. This is because the total concentration of oxLDL is still higher in the lard group. On the other hand, if corn oil doesn't reduce LDL at all relative to lard in a rhesus monkey, yet the proportion of oxLDL increases by 50%, the corn oil group will probably develop more atherosclerosis, all else being equal.

Then there are other factors that influence atherosclerosis independently of oxLDL, such as the fat-soluble antioxidants, micronutrients and omega-6:3 ratio of the diets. It's also important to keep in mind that atherosclerosis is only one factor that influences the risk of having a heart attack.

In the last post, I argued that feeding excessive cholesterol to herbivorous or nearly herbivorous animals elevates plasma LDL greatly. In many species, saturated fat exacerbates the increase in LDL due to dietary cholesterol overload. However, in the absence of added cholesterol, several commonly used models of atherosclerosis do not show an increase in LDL upon saturated fat feeding. This is similar to the situation in humans.

Rabbits are one of the most commonly used models of diet-induced atherosclerosis. They are very sensitive to dietary cholesterol, due to the fact that their natural adult diet contains virtually none.

I recently found a great study from 1967 titled "Relative Failure of Saturated Fat in the Diet to Produce Atherosclerosis in the Rabbit" (free full text). Investigators fed rabbits cocoa butter, coconut oil and Crisco (hydrogenated cottonseed oil) at 45% of calories. They found that neither cocoa butter nor Crisco increased the rabbits' cholesterol (they didn't measure LDL directly but it typically increases in proportion to total cholesterol in rabbits), while coconut oil caused a transient increase that disappeared by 6 months on the diet. Cocoa butter caused slight atherosclerosis in some of the animals while none was detected in the coconut oil or Crisco groups.

Next, the investigators fed the rabbits cholesterol along with the fats. 0.25% cholesterol with corn oil or Crisco caused a massive (10-fold) increase in blood cholesterol, and produced atherosclerosis. They didn't pair the saturated fats with cholesterol, but the point is still clear: feeding dietary cholesterol, not saturated fat, to an herbivorous species, is the culprit.

However, subsequent studies in rabbits have shown that saturated fats can produce atherosclerosis without added cholesterol. How can this be? It turns out that it only works in the context of a highly refined "synthetic" or "semi-synthetic" diet (ref). So the dietary context plays an important role as well.

The ability of saturated fat to produce atherosclerosis in animal models requires it to cause a large enough increase in serum LDL that it overwhelms saturated fat's natural tendency to reduce LDL oxidation (relative to LA). This process is typically helped along by feeding huge amounts of cholesterol. In the absence of a large increase in LDL, atherosclerosis does not result, all else being equal.

Several studies in primates support this concept. van Jaarsveld and colleagues showed that feeding vervet monkeys 28% of calories from palm oil (SFA-MUFA), sunflower oil (PUFA) or lard (MUFA-SFA) resulted in similar LDL concentrations in the three groups. After more than two years, the palm oil group had the least atherosclerosis and the sunflower oil and lard groups were similar. It's notable that palm oil was the most saturated fat used in this study.

In another telling study by Mott and colleagues, baboons were fed diets containing 40% of calories from a predominantly saturated fat or a predominantly polyunsaturated fat. Each group was further subdivided into two groups: one receiving a small amount of cholesterol in the feed, and one receiving a large amount. Cholesterol feeding increased LDL and atherosclerosis, while the type of fat had a modest effect on LDL and no effect on atherosclerosis both at high and low cholesterol levels. I've noticed that baboons seem to throw a wrench in the gears of the mainstream conception of blood lipid metabolism.

Rudel and colleagues fed african green monkeys and cynomolgus monkeys lard (MUFA-SFA) or safflower oil (PUFA) for 40% of calories, with or without added cholesterol. Without cholesterol, both LDL and the degree of atherosclerosis were low in both monkeys fed both types of fat. Cholesterol feeding raised LDL in both species by 2-3 fold, and caused significant atherosclerosis. Atherosclerosis was more severe in monkeys fed lard plus cholesterol than in monkeys fed safflower oil plus cholesterol, correlating with their considerably higher LDL.

In sum, the ability of a fat to contribute to atherosclerosis depends in part on its ability to increase oxLDL. One way to do this is to massively raise LDL. This can be accomplished by combining dietary cholesterol overload with saturated fat in certain susceptible species. Saturated fat, in the context of a somewhat normal diet, does not appear to raise LDL very much if at all in most species, in the long term. This includes humans.

Animal models of diet-induced atherosclerosis are useful for studying the disease, but they do not support the conclusion that humans should avoid foods containing natural amounts of cholesterol and saturated fat. "Saturated fats" such as lard, palm oil, beef tallow and coconut oil probably have little or no connection to atherosclerosis in humans, or in most species eating a somewhat natural diet.

Animal Models of Atherosclerosis: LDL

Researchers have developed a number of animal models of atherosclerosis (fatty/fibrous lesions in the arteries that influence heart attack risk) to study the factors that affect its development. In the next two posts, I will argue that these models rely on a massive increase in LDL, up to 10-fold, due to overloading the cholesterol metabolism of herbivorous species with excessive dietary cholesterol. This also greatly increases oxidized LDL, leading to atherosclerosis. I will discuss the role of saturated fat, which often receives the blame, in this process.

A reader recently sent me a reference to an interesting paper titled "Dietary Fat Saturation Effects on Low-density-lipoprotein Concentrations and Metabolism in Various Animal Models". It's a review of animal studies that have looked at the effect of different fats on LDL concentration as of 1997. They nail their colors to the mast in the first sentence of the abstract:

Saturated vegetable oils (coconut, palm, and palm kernel oil) and fats (butter and lard) are hypercholesterolemic [raise cholesterol] relative to monounsaturated and polyunsaturated vegetable oils.

But don't let this fool you; the actual data they present are much more interesting. First of all, they expressly exclude studies on models that have an "abnormal degree of response to a hypercholesterolemic diet". In other words, they attempt to create a self-fulfilling prophecy by excluding models that don't support their hypothesis. Even after stacking the deck, the data they present still fail to support their position.

When an investigator wants to study diet-induced atherosclerosis, first he selects a species that's susceptible to it. These are generally herbivorous or nearly herbivorous species such as rabbits, guinea pigs, hamsters, and several species of monkey. Then, he feeds it an "atherogenic diet". This is typically a combination of 0.1 to 1% cholesterol by weight, plus 20-40% of calories as fat. The fat can come from a variety of sources, but animal fats or saturated vegetable fats are typical. The remainder of the diet is processed grains, vitamin and mineral supplements, and often casein for protein.

Let's put that amount of cholesterol into human context. Assuming the average person eats about 2 pounds dry weight of food per day, 0.5% cholesterol would be 4.5 grams. That's the equivalent of:

• 17.5 pounds of beef steak, or
• 3.8 pounds of beef liver, or
• 22.5 eggs

Per day. Now feed that to an herbivore that's not adapted to clearing cholesterol. You can imagine it doesn't do their blood lipids any favors. For example, in one study, compared to a low-fat, low-cholesterol "control diet", a diet of 20% hydrogenated coconut oil plus 0.12% cholesterol caused hamsters' LDL to increase by more than 7-fold. A polyunsaturated fat (PUFA) rich diet caused LDL to increase less. This study is typical, and the interpretation is typical as well: SFA raises LDL. But there's another possibility that makes far more sense when you stand back and look at the data as a whole: in the absence of unnatural amounts of dietary cholesterol, PUFA reduces LDL in some species, and SFA has very little effect on it in most.

It's important to remember that this hamster experiment has little to do with the situation in humans. No one is claiming that reducing saturated fat and cholesterol will reduce a human's LDL by 7-fold. Long-term dietary interventions that reduce SFA and dietary cholesterol without increasing PUFA have little to no effect on LDL cholesterol, and can in fact increase LDL oxidation. Furthermore, humans are very resistant to blood cholesterol changes in response to dietary cholesterol, suggesting that we have an evolutionary history metabolizing it. Finally, as I've discussed in a previous post, saturated fat does not influence total blood cholesterol or LDL in humans in the long term, and the effects are modest even in the short term.

But let's get back to the animal models. The hypothesis the paper is attempting to support is that saturated fat raises LDL in a variety of (herbivorous) animal models. If that were true, it should be able to raise LDL even in the absence of added cholesterol. So let's consider only the studies that didn't add extra cholesterol to the diets. And if saturated fat raises LDL, it should also do it relative to monounsaturated fat (MUFA- like olive oil), rather than only in comparison to PUFA. So let's narrow the studies further to those that compared SFA-rich fats, MUFA-rich fats and PUFA-rich fats. In Fernandez et al. (1989), investigators fed guinea pigs 35% of calories from corn oil (PUFA), olive oil (MUFA) or lard (MUFA-SFA). Here's what their LDL looked like:
The same investigators published two more studies showing similar results over the next five years. The next study was published by Khosla et al. in 1992. They fed cebus and rhesus monkeys cholesterol-free diets containing 40% of calories from safflower oil (PUFA), high-oleic safflower oil (MUFA) or palm oil (SFA-MUFA). How was their LDL?
None of the differences were statistically significant. Khosla and colleagues published another study with the same result in 1993. This is hardly supportive of the idea that saturated fat raises LDL in animal models. The most you can say is that PUFA lowers LDL in some, but not all, species. There is no indication from these studies that SFA raises LDL in the absence of excessive dietary cholesterol. I didn't cherry pick studies here, I mentioned every study in the review paper that met my two criteria of no added cholesterol and a MUFA comparison group.

The bottom line is that experimental models of atherosclerosis rely on overloading herbivorous species with dietary cholesterol that they are not equipped to clear from their bodies. SFA does exacerbate the increase in LDL caused by cholesterol overload. But in the absence of excess cholesterol, it does not generally raise LDL even in species ill-equipped to digest these types of fats. Dietary cholesterol has little or no influence on LDL in humans. So there is no cholesterol overload for saturated fat to exacerbate. Consistent with this, saturated fat does not influence LDL in humans in the long term. This is contrary to the mainstream consensus, but is an inevitable conclusion if you carefully consider the evidence from controlled trials and observational studies.

PUFA vegetable oils do lower LDL in humans, and the effect appears to persist for at least a few years. But this is a Pyrrhic victory, as omega-6 PUFA increase LDL oxidation and exacerbate chronic inflammatory processes. Vegetable oils are not a solution to the coronary heart disease epidemic, to the contrary.

Experts urge use of Folic Acid before pregnancy

Folic Acid is a very important vitamin. Together with vitamin B12 it is crucial in the production of red blood cells,preventing anaemia and for the synthesis of nucleic acids (DNA). It is especially critical to the development of nerves in the foetus, and a deficiency in pregnant women is linked to birth defects such as spina bifida :http://news.bbc.co.uk/1/hi/scotland/8232089.stm

Use of Folic acid can lower the risk of Spina bifida births by up to 70%. Folic acid supplements are quite cheap to buy, so my own advice is that all women of child bearing age should take them but only by the RDA.










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Is Soya Bean good for you?

Soybeans have been found to be a storehouse of phytochemicals, beneficial antioxidant nutrients, such as saponins, phytosterols and phenolic acids, which all protect the body from free radical damage.
They are also a great source of iron, calcium and potassium.

So in health and nutrition what are Soybeans therapeutic properties?.
They will help counter heart disease, and can substantially lower blood cholesterol. In tests 8-16% over several weeks.
It can also prevent bowel diseases>

It can relieve menopausal symptoms. My wife has just started taking Soya and suffers from hot flushes so it will be interesting to see if she benefits in any way. I will keep you posted.
Soya may also have some anti-cancer activity, in particular breast cancer. Women who regularly eat Soya will find that their blood oestrogen level falls.

If you have had any experience of Soya I would be interested to know, please post your comments.
See http://www.healingdaily.com/detoxification-diet/soy.htm