Global Meat Production, 1961-2009

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Total global meat production per person has steadily increased from 0.13 lbs per day in 1961 to 0.29 lbs per day in 2009*, a 120 percent increase over the last half century (currently in the US, average meat consumption is about half a pound per day).  Since meat consumption in the US and Europe has only increased modestly over time, this change mostly reflects greatly increased meat consumption over the last half century in developing countries** in Asia, Africa and South America.  In 1961, it's likely that most of the 0.13 pounds per day of meat was consumed in affluent countries such as the US, with not much consumed elsewhere (with some exceptions).  Historically, meat has always been expensive relative to other food sources in agricultural societies, so it's eaten by those who can afford it.

The trend has been driven mostly by large increases in poultry, pork and farmed fish, while beef has declined slightly.  I suspect the doubling of pork consumption is mostly driven by Asia, because pork is the meat of choice in much of Asia, and pork intake hasn't changed much in affluent nations.  As incomes have increased in much of Asia, and food system industrialization has driven down meat prices, per capita meat consumption has increased greatly, displacing grain/legume/tuber consumption as in many other parts of the world.  This trend has not yet run its course-- per capita meat consumption is still increasing in Asia.

I'm not trying to make any grand points about the meaning of these trends for human health.  Just posting the graph because I think it's interesting to understand diet trends over time. 

These data come from the Food and Agriculture Organization, via the Earth Policy Institute data center.


* These data don't include wild fish.

** I don't like the term "developing countries" very much because it strikes me as condescending, but I don't know what else to use.

What Puts Fat Into Fat Cells, and What Takes it Out?

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Body fatness at its most basic level is determined by the rate of fat going into vs. out of fat cells. This in/out cycle occurs regardless of conditions outside the cell, but the balance between in and out is influenced by a variety of external factors.  One of the arguments that has been made in the popular media about obesity goes something like this:  


A number of factors can promote the release of fat from fat cells, including:

Epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), glucagon, thyroid-stimulating hormone, melanocyte-stimulating hormone, vasopressin, and growth hormone

 But only two promote fat storage:

Insulin, and acylation-stimulating protein (ASP)*

Therefore if we want to understand body fat accumulation, we should focus on the latter category, because that's what puts fat inside fat cells.  Simple, right?

Can you spot the logical error in this argument?

To illustrate the problem with this argument, I'll use an analogy.  When you eat food, your brain has to have a way of knowing how much has entered the body-- a feedback mechanism to keep you from overeating.  The gut secretes a variety of substances that perform this task.  These are called "satiety peptides" because they're secreted when you eat food, and they make you feel full.

Important processes like this tend to be redundant; in other words, the body does not rely on one signal to perform important tasks because if something goes wrong with that signal, you've got a problem.  There are a number of known or suspected substances that contribute to satiety, including CCK, GLP-1, amylin, PYY, glucagon, enterostatin, and others (1).  But there's one single peptide that stands out from all the others: ghrelin.  Ghrelin is the only known gut peptide that promotes food intake instead of limiting it.  When you administer ghrelin to animals or humans, they eat more and eventually gain fat** (2, 3).

But the interesting thing is that if you consider ghrelin in the proper biological context, it performs the same function as the satiety peptides: it constrains food intake***.  How is that possible?  Simple: it's regulated in a reciprocal manner to the others.  After you eat a meal, satiety peptides go up, while ghrelin plummets.  Both of these act to limit food intake.  So these two types of signals have similar effects on food intake, but they accomplish it in a reciprocal manner.

The main point I want to make here is that factors that accelerate the removal of fat from fat cells can still promote fat accumulation if they decrease, and vice versa.  All of the factors I listed at the beginning of this post can either promote or oppose fat accumulation by fat cells, depending on how they're regulated.  When you think about it that way, the picture of fatty acid trafficking in and out of fat cells suddenly becomes a lot more complicated.  You'd almost think we were complex biological systems evolved to regulate fat mass in a sophisticated and redundant manner!

One of the main control points for fatty acid trafficking is nerve terminals that enter fat tissue and release norepinephrine (nor = nerve, epinephrine = adrenaline).  Depending on the receptors expressed by fat cells, this either causes them to release or store fatty acids (most often release).  Norepinephrine is one of the dominant factors in fatty acid trafficking in/out of fat cells, and this has been universally recognized in the research community for more than half a century.

The brain is the main physiological control center of the body, and it communicates in both directions with almost every organ.  It regulates the pulse rate of the heart, breathing rate via the diaphragm, blood pressure via the blood vessel walls and kidneys, regulates temperature by controlling sweat glands, hair follicles and capillaries in the skin, regulates various aspects of digestion, bone metabolism, glucose production by the liver, insulin production by the pancreas, and many other functions.  So it's not much of a surprise that it also controls fatty acids moving into and out of fat tissue.  Nerve terminals that release norepinephrine onto fat cells are indirectly hooked up to the brain (and ultimately the hypothalamus), and it's clear at this point that the brain exerts a powerful influence on fatty acid release and storage in fat cells via these nerves (4, 5, 6). Cutting the nerves to a specific fat depot increases its size (7).  Dr. Timothy Bartness has done quite a bit of research and writing on this.

The second main point I want to make here is that the brain not only controls energy intake and energy expenditure-- factors that are obviously important determinants of fat mass-- it also influences how much fat is moving into and out of fat tissue from the circulation by acting directly on fat cells.  Viewed from this perspective, it's no wonder that the brain has consistently been an important focus of obesity research over the last 150 years, and has almost universally been recognized as the central regulator of body fat mass since the 1980s.  It's also no surprise that genetic studies have consistently turned up obesity risk factors in genes related to brain function, and the leptin signaling pathway in particular (8, 9).  And that most if not all obesity drugs act in the brain (10). 

If we want to understand the accumulation of fat in fat cells, first we have to acknowledge the complexity of the system we're dealing with.  Then, we have to look beyond the proximal factors that influence fatty acid trafficking in/out of fat cells, and look for the ultimate factors that regulate these proximal factors (i.e., what originally set the ball in motion).  Researchers understand this and have consequently been studying these ultimate factors for at least 150 years, and by far the most productive line of investigation to date has been the role of the brain.  The role of the brain in obesity is my research specialty, and I chose this field very deliberately because I recognized how important it was.  I hope to be able to convey some of this research on my blog, because not only is it fascinating, it will inoculate people against some of the odd claims circulating in the popular media. 

So as for the question I posed in the title, the answer is "a lot of things".  If it were simple, there wouldn't be thousands of people studying it full time.  Under normal conditions****, you can't just measure one factor and predict what will happen to fat cells in an intact living organism.


* Typically ASP is ignored or downplayed in these arguments, but I'm not going to open that can of worms right now. 

** Ghrelin also acts in the hypothalamus.

*** Although one could make a good argument that it's important, ghrelin's role in satiety is actually not firmly established in my opinion.  One of the main reasons is that the ghrelin receptor knockout mouse has a normal meal structure.  This may be because 1) the satiety system is so redundant that knocking out one element has no effect (this phenomenon is commonly observed in knockout animals), or 2) ghrelin really doesn't play an important role in meal termination.  I favor explanation #1, but the jury is still out.

**** With the exception of extreme cases.  For example, giving someone a shot of epinephrine, a type 1 diabetic who secretes very little insulin, a nerve to fat tissue being cut, or injecting a concentrated dose of insulin into the same fat depot for 10 years.

Symptoms Of Low Vitamin D

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It is well known now and a common fact that at any age the human body requires vitamins and minerals including calcium. Scientists and doctors documented some of the symptoms of low vitamin D include: depression, fatigue, muscle problems, osteoporosis, cancer and bones problems, general disease, weight gain, bad health and blood problems.

Diet is very important, the foods you eat is very important.

You need to get enough sun exposure to prevents low levels. But in today's world not many people can get enough sun, and that causes deficiency.

Supplements are a good way to support your body and to prevent deficiency and there are almost no side effects. You don't want to experience the symptoms of low vitamin D. When taking supplements it is important to follow the instructions, although vitamin D overdose is rare.

Blood test is an excellent way to connect low vitamin D level. A good treatment for this problem could be more exposure to sun radiation and supplements is an excellent way to insure that.

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Vitamin D Deficiency

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Vitamin and mineral d deficiency is actually characterized by hypocalcemia, hypophosphatemia, rickets in addition to osteomalacia. It is declared by measuring the exact level of 25-hydroxy-vitamin D from the blood serum. It was before uspected. Investigations uncovered undetectable levels connected with vitamin D, low serum calcium, phosphorus, in addition to increased alkaline phosphatase. Many experts have associated with improved risk of frequent cancers, autoimmune conditions, hypertension, and transmittable diseases. Vitamin d deficiency could cause depression, mental condition, fatigue, muscle cramping and diseases.

Vitamin d deficiency is often a common cause connected with bone loss within older adults. It really is an important reason behind unexpectedly low bone fragments density in individuals of any age. It may well blunt bone density result to treatment. It can be treated by using having vitamin N rich foods or maybe supplements. Vitamin n deficiency can manifest in infancy, the child years, midlife, and ageing.

Vitamin d deficiency is actually ommon and often unrecognized yet may be a key point contributing to non-connected aging. It is often a suspected risk aspect for impaired sugar tolerance and diabetes amongst adults. It is connected with low mood in addition to worse cognitive efficiency in older older people. It is frequent in older older people, and has in the past been implicated both in psychiatric and neurological diseases. Vitamin d deficiency continues to be implicated in several psychiatric mood diseases including anxiety in addition to depression.

Vitamin d deficiency continues to be linked to several sorts of cancer, including chest, prostate, colon in addition to melanoma. It offers profound effects about rat testicles, which includes dramatically reducing spermatogenesis. It is just a significant pediatric health concern, with complications which includes rickets, hypocalcemic seizures, arm or leg pain and bone fracture. It has once more become an epidemic within children, and rickets is becoming a global health concern. Vitamin d deficiency could cause rickets, which can result in permanently stunted or maybe irregular growth.

Vitamin d deficiency can result in muscle weakness and could increase the possibility of falls.

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Conclusion

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Vitamin D seems to have many results besides being associated with calcium and bone fragments health.

Some sufferers with low vitamin D levels possess fatigue and bone fragments pain, which is actually easily

reversible along with proper replacement associated with vitamin D. Vitamin D may force away heart

disease plus some types of most cancers. Vitamin D may also provide some role within regulating the

defense mechanisms and also reducing blood sugar levels levels in sufferers with diabetes. Correct

vitamin D levels are essential to prevent brittle bones. In conclusion, correct vitamin D levels

are crucial for one’s wellness, especially if you've thyroid problems. Unless someone is

exposed in order to sunlight or foods that contains vitamin D, screening with regard to Vitamin D deficiency is actually

recommended for just about all thyroid patients.

This short article is not meant to offer medical advice and it is offered for info purposes

only. Don't act or trust information from this short article without seeking expert advise.

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Keeping Fit May Reduce Breast Cancer Risk

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Women who keep fit with regular exercise, even mild physical activity, may reduce their risk of developing breast cancer, even after the menopause, but not if they also put on a lot of weight, according to a new study from the US.

The researchers found that the greatest effect was in women who exercised recreationally 10 to 19 hours a week: this appeared to reduce their risk of developing breast cancer by around 30%.

However, they also found that substantial weight gain can negate this benefit.

They write about their work in a paper due to be published this week in the journal Cancer.

Study author Lauren McCullough, a doctoral candidate at the University of North Carolina at Chapel Hill's Gillings School of Global Public Health, and colleagues, examined the effect of recreational physical activity, done at different points in life, including after the menopause, on women's risk of developing breast cancer.

While others have already shown that exercise can reduce breast cancer risk, McCullough and colleagues were interested in some of the questions that still remain unanswered. For example, how much exercise, and how often? Does it have to be intense, or does mild physical activity also have an impact? Does this work for all body types or just some? And does it work for all types of breast cancer?

For this study, they examined data on over 3,000 women aged between 20 and 98 years who took part in the Long Island Breast Cancer Study Project: a multistudy effort that began in 1993 to investigate whether environmental factors are responsible for breast cancer.

About half the women (1,504) had breast cancer, and of these the vast majority had invasive breast cancer (1,271).

The researchers found that:

* Women who exercised during their reproductive years or during the menopause had a reduced risk for breast cancer.

* Exercising 10 to 19 hours per week, outside of work activity, was linked to the largest, approximately 30%, reduction in risk.

* All levels of exercise, from mild to intense, were linked to reduction in risk of the most common breast cancers in American women, the hormone receptor positive (ER and PR positive) breast cancers.

* However, active women who gained a significant amount of weight, particularly after the menopause, had an increased risk for breast cancer, suggesting weight gain can wipe out the beneficial effect of exercise.

McCullough and colleagues did not examine the underlying reasons for the effect of exercise on breast cancer risk, but suggest it may have something to do with controlling energy balance and obesity, that leads to reduced insulin resistance and inflammation.

They conclude that:

"Collectively, these results suggest that women can still reduce their breast cancer risk later in life by maintaining their weight and engaging in moderate amounts of activity."

McCullough told the press:

"The observation of a reduced risk of breast cancer for women who engaged in exercise after menopause is particularly encouraging given the late age of onset for breast cancer."

Low vitamin D level is linked to greater chance of risk factors for Type 2 diabetes

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A new study presents more evidence of a possible link between low vitamin D levels and a higher risk of Type 2 diabetes and heart disease. The results will be presented Saturday at The Endocrine Society's 94th Annual Meeting in Houston.

The study found an inverse relationship between the level of vitamin D in the blood and the presence of the metabolic syndrome, which is a group of risk factors that increases the risk of heart disease and Type 2 diabetes. People with the highest blood levels of vitamin D had a 48 percent lower risk of having the metabolic syndrome than did those with the lowest vitamin D levels, the authors reported.

"This association has been documented before, but our study expands the association to people of diverse racial and ethnic backgrounds," said the lead author, Joanna Mitri, MD, a research fellow at Tufts Medical Center in Boston. "These include minority groups that are already at higher risk of diabetes."

Furthermore, all study participants were at risk of developing diabetes because they had prediabetes, abnormally high blood sugar levels that are not yet high enough to be classified as diabetes. Prediabetes affects an estimated 79 million Americans ages 20 or older, according to 2010 statistics from the Centers for Disease Control and Prevention.

Mitri and her co-investigators conducted the study using data from participants of the Diabetes Prevention Program, a large, now-completed study funded by the National Institutes of Health. They divided study subjects into three groups based on plasma 25-hydroxyvitamin D level, which is the most common way used to measure vitamin D status in the body, according to Mitri. The Institute of Medicine recommends a 25-hydroxyvitamin D level of 20 to 30 ng/mL as adequate for healthy people.

In the new study, the group with the highest levels of vitamin D had a median vitamin D concentration of 30.6 nanograms per milliliter, or ng/mL, and those in the lowest group had a median vitamin D concentration of 12.1 ng/mL. The risk of having the metabolic syndrome with a high vitamin D level was about one half the risk with a low vitamin D level, Mitri said.

The researchers also found an association between vitamin D status and some of the individual components of the metabolic syndrome, which includes a large waist size, low HDL ("good") cholesterol, high triglycerides (fats in the blood), high blood pressure and high blood glucose (sugar). Study participants with the best vitamin D status had a smaller waist circumference, higher HDL cholesterol and lower blood sugar.

Mitri cautioned that their research does not prove that vitamin D deficiency causes Type 2 diabetes, or even that there is a link between the two conditions.

"However, the metabolic syndrome is common, and progression to Type 2 diabetes is high," she said. "If a causal relationship can be established in ongoing and planned studies of vitamin D, this link will be of public health importance, because vitamin D supplementation is easy and inexpensive."

Treating vitamin D deficiency may improve depression

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Women with moderate to severe depression had substantial improvement in their symptoms of depression after they received treatment for their vitamin D deficiency, a new study finds. The case report series will be presented Saturday at The Endocrine Society's 94th Annual Meeting in Houston.

Because the women did not change their antidepressant medications or other environmental factors that relate to depression, the authors concluded that correction of the patients' underlying shortage of vitamin D might be responsible for the beneficial effect on depression.

"Vitamin D may have an as-yet-unproven effect on mood, and its deficiency may exacerbate depression," said Sonal Pathak, MD, an endocrinologist at Bayhealth Medical Center in Dover, Del. "If this association is confirmed, it may improve how we treat depression."

Pathak presented the research findings in three women, who ranged in age from 42 to 66. All had previously diagnosed major depressive disorder, also called clinical depression, and were receiving antidepressant therapy. The patients also were being treated for either Type 2 diabetes or an underactive thyroid (hypothyroidism).

Because the women had risk factors for vitamin D deficiency, such as low vitamin D intake and poor sun exposure, they each underwent a 25-hydroxyvitamin D blood test. For all three women, the test found low levels of vitamin D, ranging from 8.9 to 14.5 nanograms per milliliter (ng/mL), Pathak reported. Levels below 21 ng/mL are considered vitamin D deficiency, and normal vitamin D levels are above 30 ng/mL, according to The Endocrine Society.

Over eight to 12 weeks, oral vitamin D replacement therapy restored the women's vitamin D status to normal. Their levels after treatment ranged from 32 to 38 ng/mL according to the study abstract.

After treatment, all three women reported significant improvement in their depression, as found using the Beck Depression Inventory. This 21-item questionnaire scores the severity of sadness and other symptoms of depression. A score of 0 to 9 indicates minimal depression; 10 to 18, mild depression; 19 to 29, moderate depression; and 30 to 63, severe depression.

One woman's depression score improved from 32 before vitamin D therapy to 12, a change from severe to mild depression. Another woman's score fell from 26 to 8, indicating she now had minimal symptoms of depression. The third patient's score of 21 improved after vitamin D treatment to 16, also in the mild range.

Other studies have suggested that vitamin D has an effect on mood and depression, but there is a need for large, good-quality, randomized controlled clinical trials to prove whether there is a real causal relationship, Dr Pathak said.

"Screening at-risk depressed patients for vitamin D deficiency and treating it appropriately may be an easy and cost-effective adjunct to mainstream therapies for depression," she said.

'Dessert with breakfast diet' helps avoid weight regain by reducing cravings

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>Dieters have less hunger and cravings throughout the day and are better able to keep off lost weight if they eat a carbohydrate-rich, protein-packed breakfast that includes dessert. These findings come from a new study that will be presented Monday at The Endocrine Society's 94th Annual Meeting in Houston.

"The goal of a weight loss diet should be not only weight reduction but also reduction of hunger and cravings, thus helping prevent weight regain," said Daniela Jakubowicz, MD, the study's principal investigator.

Jakubowicz, a senior physician at Tel Aviv University's Wolfson Medical Center in Holon, Israel, and her co-authors studied nearly 200 nondiabetic obese adults who were randomly assigned to eat one of two low-calorie diets. Both diets had the same number of daily calories—about 1,600 for men and 1,400 for women—but differed mainly in the composition of breakfast.

One group received a low-carbohydrate diet, featuring a 304-calorie breakfast with only 10 grams of carbohydrates, or "carbs." The other group ate a 600-calorie breakfast with 60 grams of carbs, which included a small sweet, such as chocolate, a doughnut, a cookie or cake. Both diets contained protein (such as tuna, egg whites, cheese and low-fat milk) at breakfast, but the "dessert with breakfast diet" had 45 grams of protein, 15 grams more than in the low-carb diet.

Halfway through the eight-month study, participants in both groups lost an average of 33 pounds (15.1 kilograms, or kg) per person, which Jakubowicz said shows that "both diets work the same." However, in the last four months of the study, the low-carb group regained an average of 22 pounds (11.6 kg) per person, while participants who ate the dessert with breakfast diet lost another 15 pounds (6.9 kg) each, the authors reported.

In addition, the study subjects who ate the dessert with breakfast diet reported feeling less hunger and fewer cravings compared with the other group. Subjects' food diaries showed that the dessert with breakfast group had better compliance in sticking to their calorie requirements. Women who ate the dessert with breakfast diet were allowed 500 calories for lunch and about 300 calories for dinner. Men in that group could eat a 600-calorie lunch and up to 464 calories at dinner.

As further evidence supporting the dessert with breakfast diet, the levels of ghrelin, the so-called "hunger hormone," dropped much more after breakfast than in the low-carb group: 45.2 percent versus 29.5 percent, respectively, according to the abstract.

Jakubowicz attributed the better results from the dessert with breakfast diet to meal timing and composition. She said the diet's high protein content reduced hunger; the combination of protein and carbs increased satiety, or feeling full; and the dessert decreased cravings for sweet, starchy and fatty foods. Such cravings often occur when a diet restricts sweets and can result in eating many fattening foods that are not allowed on the diet, she said.

This study was published in the March issue of the journal Steroids.

Low vitamin D levels linked to weight gain in some older women

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Kaiser Permanente study finds most older women have insufficient levels of the 'sunshine vitamin'

Older women with insufficient levels of Vitamin D gained more weight than those with sufficient levels of the vitamin, according to a new study funded by the National Institutes of Health and published online today in the Journal of Women's Health. The study of more than 4,600 women ages 65 and older found that over nearly five years, those with insufficient levels of Vitamin D in their blood gained about two pounds more than those with adequate levels of the vitamin.

"This is one of the first studies to show that women with low levels of Vitamin D gain more weight, and although it was only two pounds, over time that can add up," said study author Erin LeBlanc, MD, an endocrinologist and researcher at the Kaiser Permanente Center for Health Research in Portland, Oregon. "Nearly 80 percent of women in our study had insufficient levels of Vitamin D. A primary source of this important vitamin is sunlight, and as modern societies move indoors, continuous Vitamin D insufficiency may be contributing to chronic weight gain."

Vitamin D was in the news recently when a panel of primary care experts-- the US Preventive Services Task Force-- said healthy postmenopausal women may need higher doses of the vitamin to prevent fractures, and that there isn't enough evidence to recommend the supplements for younger people. Other expert groups, including The Endocrine Society, have a different take, saying many adults do need Vitamin D supplements to keep their bones healthy. 1

"Our study only shows an association between insufficient levels of Vitamin D and weight gain, we would need to do more studies before recommending the supplements to keep people from gaining weight," LeBlanc said. "Since there are so many conflicting recommendations about taking Vitamin D for any reason, it's best if patients get advice from their own health care provider."

She points out that this study was conducted among older women who, for the most part, were not trying to lose weight—though some of them did so as a natural result of aging. About 60 percent of the 4,659 women in the study remained at a stable weight (within 5 percent of their starting weight) over the 4.5-year study period, 27 percent lost more than 5 percent of their body weight, and 12 percent gained more than 5 percent of their body weight.

Most women in the study (78 percent) had less than 30 nanograms per millimeter (ng/ml) of Vitamin D in their blood—the level defined as sufficient by The Endocrine Society panel of experts who set clinical guidelines on Vitamin D deficiency. These women had higher baseline weight to begin with: 148.6 pounds, compared with 141.6 pounds for women whose Vitamin D levels were 30 ng/ml or above. Insufficient levels had no association with weight changes in the entire group of women, or in the group that lost weight. But in the group of 571 women who gained weight, those with insufficient Vitamin D levels gained more—18.5 pounds over five years—than women who had sufficient Vitamin D. The latter group gained 16.4 pounds over the same period.

Flaxseeds For Men's Fertiliy

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Overcome Male Infertility - How to Treat Infertility With Flaxseed

Guest Post By Kyle J Norton


As we mentioned in previous articles, infertility is defined as inability of a couple to conceive after 12 months of unprotected sexual intercourse. It effects over 5 millions couple alone in the U. S. and many times more in the world. Because of unawareness of treatments, only 10% seeks help from professional specialist.We have spent most of the time in this series discussing the conventional and Chinese medicine in treating fertility. I believe, it is the best time to change the subject by discussing how to treat male infertility with flaxseed oil.
I. Definition

Flax, also known Linum usitatissimum, is a member of the genus Linum. Belonging to the family Linaceae, it's seed has been used in traditional medicine in treating heart diseases caused by high levels of cholesterol.
II. How flaxseed oil effects male fertility

1. Essential fatty acid

Flaxseed oil contains high levels of essential fatty acid Omega 3 and 6, it not only help to eliminate the trans fat and saturate fat through liver waste elimination, but also helps to increasing blood flow to the reproductive organs resulting in increasing the production of sperm count and sperm quality.
2. Lignan

flaxseed contains high amount of ligan, it is proven in helping to strengthen not only the immune system in fighting against irregular cells growth, but also improve it's function in protecting the body own tissues, including sperm.
3. Lecithin

Lecithin is a fat like substance (phospholipid) found in flaxseed not only helps to inhibit the levels of bad cholesterol, but also is a key building block of cell membranes resulting in protecting protects cells from oxidation in the surrounding the brain, thus lessening the risk of nervous tension, hormone imbalance and low libido.
4. Fiber

Flax seeds contain high amount of fiber which is vital in helping liver in regulating spleen in insulin production, resulting in decreasing the risk of blood stagnation and qi imbalance in spleen, leading to normalizing the production of testosterone and increasing the chance of good quality sperm production.
5. Alpha linolenic acid

It also contains high levels of alpha linolenic acid which is vital for a healthy prostate gland, resulting in increasing the kidney function in regulating sperm production as well as strong ejaculation.
III. Side effects

1. Intestinal blockage, if it is taken in large amounts. Please remember to drink a lot of liquids to avoid this to happen.

2. Because of it' high concentration of fiber, it may reduce the effectiveness of some oral medicine.





For the best pregnancy self help program review, please visit http://bestfertility.blogspot.com/.
For series of Infertility Articles, please visit http://fertility-infertility.blogspot.com/.
All rights reserved. Any reproducing of this article must have the author name and all the links intact.
"Let You Be With Your Health, Let Your Health Be With You" -Kyle J. Norton
I have been studying natural remedies for disease prevention for over 20 years and working as a financial consultant since 1990. Master degree in Mathematics, teaching and tutoring math at colleges and universities before joining insurance industries. Part time Health, Insurance and Entertainment Article Writer.


Article Source: http://EzineArticles.com/?expert=Kyle_J_Norton


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Vaginal Lubricants & Fertility: Vegetable Oil?

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I think most of us know to stay away from vaginal lubricants when trying to conceive. However, the study cited below shows that there are some sperm friendly vaginal lubricants including cannola oil (skip the vinegar!) Read more:

Vaginal lubricants for the infertile couple: effect on sperm activity.

From the study:

MAIN OUTCOME MEASURES: Sperm motility was evaluated by manual motility counts and by computer-assisted semen analysis. Sperm viability was evaluated with Hoechst 33258 dye. The effects of the various lubricants were compared with those of a spermicidal agent, Gynol II (negative control) and Ham's F-10 (positive control). RESULTS: Commercial lubricants inhibited sperm motility by 60-100% after 60 minutes of incubation. Sperm exposed to Replens or Astroglide were nonmotile and nonviable after incubation for 60 minutes, similar to the control, nonoxynol-9 containing product Gynol II. Canola oil had no detrimental effects and was indistinguishable from Ham's F-10 in terms of sperm viability and motility.

Why Triclosan Hurts Fertility and Other Dangers Of Antibacterial Agents

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I talk in my book about how you should avoid some hand sanitizers if you are trying to conceive - especially those with triclosan. Triclosan can be quite dangerous and it is in a number of consumer products, not just hand sanitizers. Please read the labels and do your research! I was surprised to find out that triclosan isn't just a hormone disruptor, it's also a carcinogen. Yikes!

www.townsendletter.com

From the article:

The EPA considers triclosan a high risk for human health and the environment. When introduced in 1972, triclosan was confined to health care settings in a surgical scrub.1-4

Triclosan may not be a familiar term to most consumers, though it is now ubiquitous in most American households, masquerading under the unassuming term, "antimicrobial." In the United States, "antimicrobial" has become synonymous with cleanliness and good health. The chemical industry has fostered a fear of germs among American consumers and developed a lucrative market selling products designed to protect us from germs. The EPA estimates sales of antimicrobial products now constitute a billion dollar per year industry...

...The chemical structure of triclosan resembles certain estrogens. One study on a species of Japanese fish did not indicate any estrogenic effects, but found androgenic effects resulting in changes in fin length and sex ratios.2

Triclosan is lipophilic, attaching to fatty tissue. It can accumulate in the liver, lungs, and kidneys, reaching toxic levels. As a chlorophenol, it is categorized as a persistent organic pollutant, along with dioxins and PCBs. These chemicals persist in the environment and bioaccumulate up the food chain. Being at the top of the food chain, humans harbor the most concentrated amounts of these toxic chemicals.2-4

Triclosan's use is already so widespread it has made its way into the human body. Studies show triclosan residues in the umbilical cord blood of infants and in the breast milk of nursing mothers.9 Triclosan has not been thoroughly tested nor evaluated for potential risks to human health and the environment though it is in a category of very toxic and carcinogenic chemicals. It is chemically similar to Agent Orange.

Pregnant Naturally With Alternative Treatments

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This YouTube video from www.hunyuan.org is a testimonal about a couple who had been told their chances of conceiving were slim to none. They followed an all natural program and got pregnant naturally despite the odds. Her testimonial is more proof that there is hope even in extreme circumstances. I hear from women every day who supposedly beat the odds (but I'm not sure what the "odds" are based on!)

Yes, Daily Intercourse Helps Sperm Quality

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The amount of intercourse recommended if a couple is trying to conceive has been debated.
I've read countless articles which say every day, every other day, etc. etc. etc.

This article seems to support having intercourse every day up to a week before ovulation. There seems to be value in moving the sperm through the male reproductive system so there is always a new fresh supply. Read more:

www.sciencedaily.com

From the article:

we found that although frequent ejaculation decreased semen volume and sperm concentrations, it did not compromise sperm motility and, in fact, this rose slightly but significantly.

“Further research is required to see whether the improvement in these men’s sperm quality translates into better pregnancy rates, but other, previous studies have shown the relationship between sperm DNA damage and pregnancy rates.

“The optimal number of days of ejaculation might be more or less than seven days, but a week appears manageable and favourable. It seems safe to conclude that couples with relatively normal semen parameters should have sex daily for up to a week before the ovulation date.

Breastfeeding Mothers Who Exercise: Risk or Benefit When It Comes to Milk Production?

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Over the years, a few studies have appeared in the peer-reviewed literature suggesting that a breastfeeding mother who exercises may reduce the amount of breast milk produced and in turn hamper the growth of her infant. Fortunately, Daley et al. (doi: 10.1542/peds.2011-2485) decided to look systematically at this issue by looking only at randomized controlled trials (RCTs) using a variety of search engines to identify appropriate studies. Unfortunately only 4 RCTs qualified but the results are certainly not worrisome and do not support discouraging breast feeding women from exercising. For more details, consider giving this review article your attention — and if you read it while on the treadmill — all the better.

Planning Improvement

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Our Quality Reports Editor Dr. Alex Kemper offers the following preview of what’s being published in the newest section of our journal:

Volpe et al. (doi: 10.1542/peds.2012-0153) present an important project to improve the timeliness of antibiotic delivery for febrile neutropenic patients n the emergency department setting. I think there is an important "take home" point even for those who practice outside of the emergency department or who are unlikely to care for severely immunocompromised children. First, Volpe et al. spent a significant amount of time and energy planning their intervention. Without such work, attempts to improve quality are likely to fail. Their report does a great job describing process maps, and the resulting key driver diagram (figure 2) beautifully illustrates their goal, the challenges, and their approaches to improvement. In my experience, this up-front work is skipped over by inexperienced individuals engaged in quality improvement, usually to the detriment of the project.

Recovery Times

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Dr. William V. Raszka, our Associate Editor, offers the following insight into a current topic in the news:

At dinner the other night, my wife and I were talking with our neighbor about marathon running. She is an avid runner, and ran in the Boston Marathon. When I asked her if she planned to run another marathon this year she replied that it takes too long to recover and that she would not compete in another for a long time. However, my wife’s sister, roughly the same age and also an avid runner, will compete in six marathons this year. How is it that one avid runner can only compete in one marathon each year while another can compete in six?

As reported in The New York Times (Health: March 19, 2012), how long it takes to recover from a marathon or any other strenuous exercise is not known and is dependent on a host of factors including the mental state of the runner. A popular theory is that the recovery time in days is equal to the number of miles run (e.g., it will take 20 days to fully recover from a 20 mile running race). However, this is not based on any scientific studies and seems mostly discredited by the athletic community. One of the challenges is defining what recovery means. Recovery can mean absence of soreness, replenishment of muscle glycogen, return to peak performance, or even psychological well-being. No benchmarks for any of these exist. We do know that athletes who consume carbohydrates or a bit of protein after exercise seem to replenish muscle glycogen stores with 24 hours or so. Most muscle soreness resolves within a week.

However, muscle soreness that prevents exercise leads to deconditioning so that it takes additional time to be able to return to the same performance level. For others, the emotional toll can exceed the physiologic one. Many elite marathoners only run one or two marathons a year as it can take months to recover from the effort. The reasons for the apparent difference in recovery times between my neighbor and sister-in-law may lie in their reason for running in the first place. My neighbor, having met the time she wanted, feels that the pain associated with marathons outweighs any potential joy. My sister-in-law, however, runs to prove something to herself and her family so she will be on the roads within days of finishing the marathon.

Noted by WVR, MD

*This filler excerpt can be found in the June 2012 Pediatrics print journal p. 1110, or via online here.

Taking a Shot at the Alternative Vaccine Schedule: Is Anyone Really Using It?

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It seems that the media finds much more to talk about when it comes to wanting to find fault with vaccinations rather than herald their benefits. Yet, vaccines are probably one of the most important if not the most important contribution to public health of the 20th and 21st centuries. Despite this contribution, some parents are not convinced that the benefits of vaccinating on time outweigh the risks, and in some circumstances pediatricians and family physicians have had to “compromise” and provide a delayed “alternative” vaccination schedule, one not recommended by the AAP or the Advisory Committee on Immunization Practices of the Centers for Disease Control (ACIP). So how popular is using a non-recommended schedule? Robison et al. (doi: 10.1542/peds.2011-3154) address this question by studying vaccine compliance in Portland Oregon from 2004-2009. The authors used a retrospective cohort analysis of a vaccine registry to look at prevalence trends for use of an alternative schedule — taking into account the 2007-2009 Hib shortage and increased availability of combination vaccines. While the overall prevalence is just under 5%, the rate almost doubled in the latter years of this study, suggesting that more families are opting out of receiving the recommended vaccines in a timely fashion. This study only looks at one urban area, and it remains to be seen whether this will result in more break-through cases of pertussis and other preventable illnesses in the Portland area. Certainly, this is a realistic concern given the trends reported in this important article.

Waiting Well

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Dr. William V. Raszka, our Associate Editor, offers the following insight into a current topic in the news:
Last week I had dinner two nights in a row at a well-known restaurant in a city I was visiting. Both evenings were quite pleasurable as I was dining with old friends. However, I left dinner the first night a bit disappointed with the restaurant, while the second night I left reasonably content. Upon reflection, the disparate feelings had nothing to do with the food but with the wait staff. On both evenings, the wait person had introduced him or herself, offered drinks, and pushed specials (or food treatments) without disclosing their prices-practices with which I am quite familiar. However, while the waiter on the first night often interrupted our conversation, whether by interjecting or standing tableside until we stopped talking, the waitress the second night quickly grasped that we wanted some time to ourselves and uninterrupted conversation. She told us how to signal when we wanted additional service and left us to our devices.

According to an article in The Wall Street Journal (Business: February 22, 2012), the wait-staff’s ability to “read” a table of diners correctly takes training. Restaurants are interested in providing superior, personalized service (as the food or décor in different restaurants can be quite similar) but people and the personal experience cannot be replicated. With the number of diners at restaurants expected to only grow about 1% over the next several years, restaurants at all price points are increasingly competing not just on food but on service as well. Inexperienced wait-staff can expect one- or even two-week long training sessions that emphasize not only how to recite food items, but how to make eye contact, decide to whom to give the dessert menu (usually the mother if children are involved), and determine who wants fast (early diners dressed quite well) or slower (diners that actively engage the wait-staff) service. Wait-staff are also trained to use situational selling of alcohol, appetizers, desserts, or other food products based on the dynamic of the table rather than follow uniform scripts.

When to bring the check to the table seems to be the most difficult task for wait staff-so difficult that at least one restaurant chain has developed check holders that signal when the diner wants the bill and when the bill has been settled. As for me, I left the restaurant the second night quite happy that I had been able to share a lovely dinner with friends. The waitress had been unobtrusive but quite responsive, and I showed my appreciation by leaving a large tip.


Noted by WVR, MD
*This filler excerpt can be found in the June 2012 Pediatrics print journal p. 1124, or via online here.

Lessons From Ötzi, the Tyrolean Ice Man. Part I

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This is Otzi, or at least a reconstruction of what he might have looked like.  5,300 years ago, he laid down on a glacier near the border between modern-day Italy and Austria, under unpleasant circumstances.  He was quickly frozen into the glacier.  In 1991, his slumber was rudely interrupted by two German tourists, which eventually landed him in the South Tyrol Museum of Archaeology in Italy. 

Otzi is Europe's oldest natural human mummy, and as such, he's an important window into the history of the human species in Europe.  His genome has been sequenced, and it offers us clues about the genetic history of modern Europeans.

Otzi's Story


Due to his amazing state of preservation, researchers have been able to learn a lot about Otzi's life.  Based on an analysis of his tooth enamel and pollen grains found on his clothing, we know that Otzi grew up near the modern-day Italian village of Feldthurns, but later migrated to the valleys about 50 kilometers North of there (1).  He was probably involved in copper smelting, judging by the high levels of copper and arsenic in his hair.

On the day he died, Otzi was wearing skillfully crafted leather shoes lined with grass, a leather coat, leggings, a loincloth, a bearskin hat, and a cloak made of woven grass.  He also carried a valuable copper axe, a flint knife, a fire kit, a bow and flint-tipped arrows.  Otzi was an affluent but rugged mountain man armed to the teeth!

Otzi died in an armed struggle while away from home.  He was shot in the back by a flint-tipped arrow, which severed an internal artery and would have been fatal (2).  His body was probably turned over by his killers, who retrieved the arrow (sans arrowhead).  He also sustained a head wound, which may have been due to a fall or a deliberate blow.  Unpublished DNA evidence suggests that his body had the blood of four other people on it-- two on an arrowhead, one on his knife, and one on his coat (3).  Since he died outside his home territory, some have speculated that he was part of a raiding party.  He likely killed or wounded several others and then was himself killed.  Such was the life of prehistoric males.

In the next post, I'll describe Otzi's diet, and what we know about his health.

Next Primal Chef Event Sunday 5/20

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Gil Butler has been working on a television show called Primal Chef, where he invites local chefs to make creative dishes from a list of Paleo ingredients, in a designated amount of time.  The format is reminiscent of Iron Chef.  The food is judged afterward by figures in the Paleo community.  Robb Wolf was a judge on the first episode.

Gil has invited me to be a judge on the next show, along with Sara Fragoso and Dr. Tim Gerstmar.  The next day, Sunday April 20th, Gil is organizing a catered Primal Chef event in Seattle, with Paleo dinner, speakers, entertainment, prizes, and a screening of part of Paleo Chef episode 1.  You can read the details and sign up here.  I won't be speaking because I don't have time to put together another talk right now, but I will be attending the event. 

Exercise and Food Intake

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The New York Times just published an article reviewing some of the recent research on exercise, food intake and food reward, titled "Does Exercise Make You Overeat?".  I was planning to write about this at some point, but I don't know when I'd be able to get around to it, and the NYT article is a fair treatment of the subject, so I'll just point you to the article.

Basically, burning calories through exercise causes some people to eat more, but not everyone does, and a few people actually eat less.  Alex Hutchinson discussed this point recently on his blog (1).  Part of it depends on how much fat you carry-- if you're already lean, the body is more likely to increase hunger because it very much dislikes going too low in body fat.  Most overweight/obese people do not totally make up for the calories they burn through exercise by eating more, so they lose fat.  There is a lot of individual variability here.  The average obese person won't lose a substantial amount of fat through exercise alone.  However, everyone knows someone who lost 50+ pounds through exercise alone, and the controlled trials support that it happens in a minority of people.  On the other side of the spectrum, I have a friend who gained fat while training for a marathon, and lost it afterward. 

Recent studies, reviewed in the NYT article, have shown that one of the key determinants of who eats more and who doesn't is the activation of reward circuits in the brain.  From a neurobiology perspective, these are THE circuits that determine your motivation to seek and consume food.  People who have increased reward circuit activation after exercise eat more; people who have less reward circuit activation after exercise eat less.  It's nothing revolutionary, because it's exactly what you'd expect, but it's still nice to see it confirmed.

Here's a quote from the end of the article:

“Four or five years ago, it really looked like appetite hormones” controlled what we eat, says Dr. Habogian, who conducted some of the first studies of exercise and the hormones. “But I’m more and more convinced that it’s the brain. Hormones don’t tell you to go eat. Your brain does. And if we can get the dose right, exercise might change that message.”

Of course, hormones and other circulating signals influence what the brain decides, so they do have a substantial impact.  But the brain is the ultimate arbiter of food intake behaviors, and hormones and other circulating signals are among many factors that it considers.  I'll be exploring this in more detail in coming posts.

Lessons From Ötzi, the Tyrolean Ice Man. Part II

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Otzi's Diet

Otzi's digestive tract contains the remains of three meals.  They were composed of cooked grains (wheat bread and wheat grains), meat, roots, fruit and seeds (1, 2).  The meat came from three different animals-- chamois, red deer and ibex.  The "wheat" was actually not what we would think of as modern wheat, but an ancestral variety called einkorn.

Isotope analysis indicates that Otzi's habitual diet was primarily centered around plant foods, likely heavily dependent on grains but also incorporating a variety of other plants (3).  He died in the spring with a belly full of einkorn wheat.  Since wheat is harvested in the fall, this suggests that his culture stored grain and was dependent on it for most if not all of the year.  However, he also clearly ate meat and used leather made from his prey.  Researchers are still debating the quantity of meat in his diet, but it was probably secondary to grains and other plant foods. It isn't known whether or not he consumed dairy.

Otzi's diet would have been high in carbohydrate, mostly from einkorn wheat (and perhaps other grains) but also from fruit and possibly legumes.  It was probably moderate in protein, with the protein coming from grains, perhaps legumes and some meat.  He probably didn't eat much fat, but he did get some fat from nuts and meat.

Otzi's Health

Otzi was about 45 years old at the time of his death, had a lean and fit physique, and stood roughly 5 feet, 5 inches tall (1.65 m).  This adult male height is typical of hunter-gatherers and other non-industrial people throughout the world today (except those that rely heavily on dairy), but that's a topic for another post. 

Otzi was not exactly the picture of health.  He suffered from a number of health problems, both infectious and non-infectious in nature. 

Like nearly all non-industrial populations, Otzi probably had intestinal parasites; in his case, his colon contained whipworm eggs (4).  Lines in his fingernails showed signs of an unknown illness that occurred three times in the four months before his death.  His body also bears DNA evidence that he may have been infected with Lyme disease, a serious chronic bacterial infection transmitted by tick bites (5).

Otzi's body also shows signs of a number of non-infectious disease processes.  Several of his major arteries were calcified-- suggesting advanced vascular disease that's normally associated with an elevated heart attack risk.   He had three gallstones, which has been used to support the idea that he ate a lot of animal fat, but this seems like a major leap of faith to me.  He had arthritis in several locations, including the spine and hips (6).  He had cavities and periodontitis (6a).  His lungs were blackened, presumably from the smoke of fires used for various purposes, including smelting copper.

Perspective

Otzi is probably fairly representative of early agriculturalists in some ways, and to a lesser extent, the hunter-gatherers that preceded him.  The archaeological (skeletal) record shows evidence of severe physical stress in early agriculturalists, including short stature, cavities, and skeletal abnormalities, which probably reflect both nutritional and infectious stress (Cohen and Crane-Kramer. Ancient Health. 2007; Cohen. Health and the Rise of Civilization. 1991).

The shift to agriculture involved a major change in diet, away from a hunter-gatherer diet composed of diverse wild plant and animal foods, to a diet centered around grains.  Although some humans may have eaten grains for tens of thousands of years before domesticating plants, grains clearly became a more central source of food during the Neolithic. This posed a number of nutritional problems that would have exerted selective pressure over time, favoring genetic adaptations to the new diet.  Later agriculturalists were taller and healthier than early agriculturalists, probably due to a combination of genetic and cultural adaptations (Cohen and Armelagos. Paleopathology at the Origins of Agriculture. 1984).

The more sedentary lifestyle, higher population density, and contact with livestock associated with agricultural life created new opportunities for human pathogens (Cohen. Health and the Rise of Civilization. 1991).  A number of parasites, bacteria and viruses took advantage of the situation, becoming more diverse and virulent and giving rise to many of the most problematic infectious diseases we know today.  These new infectious threats were extremely debilitating and deadly for early adopters of agriculture in Eurasia, just as they were for unexposed populations when Europeans reached the Americas.  However, the strong selective pressures they exerted on the ancestors of modern Eurasians gave rise to a number of protective genetic adaptations, the traces of which are highly visible in our modern genomes. 

Otzi's health is clearly not something to aspire to.  In some ways, it's representative of contemporary hunter-gatherers and non-industrial agriculturalists: his leanness and probable lack of metabolic disorders such as diabetes, as well as the presence of intestinal parasites and other infectious diseases.  In other ways, some of the findings are surprising: his cardiovascular disease and gallstones, which are considered "diseases of affluence" today.

I think we have to take the cardiovascular disease with a grain of salt.  Modern-day non-industrial agriculturalists typically have low levels of atherosclerosis (a thickening and degeneration of the vascular wall) compared with affluent nations, even if the diet is grain-heavy, although they are not free from atherosclerosis (7).  No one knows how much atherosclerosis hunter-gatherers have, because no one has ever done cardiac autopsies to my knowledge.  But we do know they have low blood pressure, low circulating lipids, and high physical fitness, which argues against the presence of serious vascular disease.  Otzi was exposed to high levels of copper and arsenic from smelting, particulate matter from smoke, and Lyme disease.  He also had a genetic predisposition to cardiovascular disease, which I'll discuss later.  It's likely that at least some of these factors contributed to his cardiovascular disease, and in addition it's hard to know how representative he was of his culture.

The other thing to keep in mind is that having atherosclerosis doesn't necessarily mean a person will have a heart attack.  There are other important components of risk, including the tendency of the blood to clot, the tendency of the heart to enter fibrillation (irregular contraction that can be fatal), blood vessel diameter, and the stability of plaque in the artery wall.  These may explain why some non-industrial populations have a much lower heart attack risk than would be predicted from their degree of vascular disease (8).  The point is that just because Otzi had signs of advanced atherosclerosis, does not necessarily mean he was about to have a heart attack.

In the next post, I'll delve into Otzi's genome, and the insights it contains into the evolution and health of modern Europeans.

A Pressure Cooker for the 21st Century

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Pressure cookers are an extremely useful kitchen tool.  They greatly speed cooking and reduce energy usage by up to 70 percent.  This is because as pressure increases, so does the boiling point of water, which is the factor that limits cooking speed in water-containing foods (most foods).  If it weren't for my pressure cooker, I'd rarely eat beets or globe artichokes.  Instead of baking, boiling or steaming these for 60-90 minutes, I can have them soft as butter in 30.  But let's face it: most people are intimidated by pressure cookers.  They fear the sounds, the hot steam, and the perceived risk of explosion.  I escaped this because I grew up around them.

Recently, I was looking for a new pressure cooker to replace my abused old Presto.  I had my sights set on a modern "second generation" stainless steel model.  But looking around a bit more, I discovered that pressure cookers have evolved quite a bit in the last decade.  There's actually a "third generation" now: the electronic pressure cooker.  These not only pressure cook, they also slow cook, make rice, and can also brown meats/vegetables for stews.  They're even more efficient than traditional pressure cookers because they're insulated and release very little steam.  And they cook quietly, at the push of a button, while you do something else.

Of course I had to have one.  There are a number of models available, but I only found one that has a stainless steel insert rather than nonstick.  I don't really know whether nonstick is a health risk or not-- honestly I doubt it-- but I'm not going to do the experiment on myself.  Stainless steel is also more durable than nonstick, and durability is extremely important to me for both financial and environmental reasons. 

The model I found is called the Instant Pot LUX-60.  It seems to be marketed mostly to Asians (e.g., it has a congee setting), but it's perfectly adaptable to the Western kitchen.  I received it two months ago, and we've been using it several times a week since then.  It appears to be solidly built, and I expect it to last a long time.  The insert is fairly substantial stainless steel that has a 3-ply bottom for even heat distribution, and the gaskets are all made of durable silicone.

It's amazing how many things you can cook in it.  It fits a whole chicken, which cooks in 45 minutes (vs. 1.5 hours in the oven).  Rich soup stock from the bones takes 40 minutes.  Pre-soaked chickpeas are very tender in 25 minutes.  Pot roast in an hour and a half.  Four cups of rice cooks in under 30 minutes and comes out better than when I make it in my rice cooker.  All you have to do is press a couple of buttons and you're done.  Cleanup is a breeze.  I was initially concerned that the higher temperature would cause nutrient loss, but the reading I've done seems to indicate that it compares favorably to other cooking methods.

I'm always on the lookout for tools that allow busy people to cook at home in a more efficient manner, encouraging a wholesome and economical diet rather than relying on commercially prepared food.  This pressure cooker definitely qualifies.  I'm sold on this thing.  Can you tell?  My friends are getting tired of hearing me rave about it.  I promise Instant Pot didn't pay me to write this.

Lessons From Ötzi, the Tyrolean Ice Man. Part III

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There are two reasons why I chose this time to write about Otzi.  The first is that I've been looking for a good excuse to revisit human evolutionary history, particularly that of Europeans, and what it does and doesn't tell us about the "optimal" human diet.  The second is that Otzi's full genome was sequenced and described in a recent issue of Nature Communications (1).  A "genome" is the full complement of genes an organism carries.  So what that means is that researchers have sequenced almost all of his genes. 


I have a background in genetics, but genetic anthropology is complicated and it isn't my field.  Some of what I'll present in coming posts is still vigorously debated in anthropology circles, and I don't know the details of all the arguments.  I'll do my best to present the science as I understand it, and if you happen to be a genetic anthropologist and you have a different perspective, please share it in the comments.

Otzi's Mitochondrial Genome

The first genetic information we have about Otzi predates the recent paper by 18 years.  Mitochondria are the cell's tiny power plants, and they have their own tiny genome that's passed down through the maternal lineage.  In 1994, a German group published the first analysis of his mitochondrial genome, indicating that Otzi is genetically related to present-day Europeans (2).  Later papers described his full mitochondrial genome (3, 4). 

Modern-day people are divided into mitochondrial "haplogroups", which simply indicates relatedness through the maternal lineage.  What these papers found is that Otzi belongs to haplogroup K, a haplotype that's present in about 6 percent of people in Europe and the Near East today.  Haplogroup K originated about 16,000 years ago near the cradle of agriculture in the Middle East, and spread outward from there.  It has been found in the remains of early agricultural populations in the Middle East and Europe (5, 6, 7, 8).

These mitochondrial studies indicate that Otzi was, at least in part, a genetic migrant descended from early agriculturalists in the Middle East, rather than a full descendant of local hunter-gatherer populations in Europe that adopted agriculture over time. 

Otzi's Nuclear Genome

The "nuclear genome" is the complement of genes that's contained in the nucleus, and it represents by far the lion's share of a person's genetic material.  This is what the recent paper reported sequencing (9).  It contains a number of insights:

• Otzi is most closely related to modern-day Sardinians.
• Otzi had several genetic cardiovascular disease risk factors that collectively would have put him at a substantially elevated risk of having a heart attack or stroke.  This may explain his vascular disease, at least in part.
• Otzi probably had Lyme disease, a chronic and serious bacterial infection transmitted by ticks.
• Otzi probably had brown eyes.
• Otzi was lactose intolerant.
• "...Otzi carried a large genomic region known as the ‘Y chromosome’, which significantly increases the risk of traipsing about in the a*se-end of nowhere with very little protective clothing, and getting shot by arrows" (10)

In addition, his Y chromosome indicated that his paternal lineage (haplogroup G) also has roots in early agricultural populations in the Middle East.  This is the same lineage that has been found in other early agricultural remains in Europe (11).  This is consistent with his mitochondrial genome and indicates that he descended in large part from early adopters of agriculture in the Middle East.

Why do We Care about Otzi's Genome?

I'm going to begin to answer that question with a question.  What was a man of Middle Eastern agriculturalist descent doing on the border of Italy and Austria 5,300 years ago?  And what were genes originating from early Middle Eastern agriculturalists doing in many other parts of Europe as early as 8,000 years ago (12)?  These findings, among many others, suggest that agricultural populations from the Middle East not only brought their subsistence strategy to Europe, they also brought their genes. 

Researchers have found that Paleolithic humans and neanderthals in Europe had a diet that was heavily focused on meat (13, 14), and this has been used to suggest that modern-day people of European descent should eat a meat-heavy, low carbohydrate diet to mimic their own ancestral dietary pattern.  But this makes a big assumption: that those Paleolithic meat eaters were the ancestors of modern-day Europeans. If instead, modern Europeans descend from Middle Eastern agriculturalists who originally came from Africa, that means they were never hunter-gatherers in Europe and therefore never ate a diet focused on meat and fat-rich large temperate game.  If they descended from Middle Eastern agriculturalists who ate a high-carbohydrate grain-based diet for some 10,000 years, this may lead to different conclusions about the ancestral European diet.

In future posts, I'll explore what research has uncovered about European ancestry, human evolution since the development of agriculture, and what that means for the human dietary niche. 

Beyond Ötzi: European Evolutionary History and its Relevance to Diet. Part I

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In the previous post, I explained that Otzi descended in large part from early adopters of agriculture in the Middle East or nearby.  What I'll explain in further posts is that Otzi was not a genetic anomaly: he was part of a wave of agricultural migrants that washed over Europe thousands of years ago, spreading their genes throughout.  Not only that, Otzi represents a halfway point in the evolutionary process that transformed Paleolithic humans into modern humans.

Did Agriculture in Europe Spread by Cultural Transmission or by Population Replacement?

There's a long-standing debate in the anthropology community over how agriculture spread throughout Europe.  One camp proposes that agriculture spread by a cultural route, and that European hunter-gatherers simply settled down and began planting grains.  The other camp suggests that European hunter-gatherers were replaced (totally or partially) by waves of agriculturalist immigrants from the Middle East that were culturally and genetically better adapted to the agricultural diet and lifestyle.  These are two extreme positions, and I think almost everyone would agree at this point that the truth lies somewhere in between: modern Europeans are a mix of genetic lineages, some of which originate from the earliest Middle Eastern agriculturalists who expanded into Europe, and some of which originate from indigenous hunter-gatherer groups including a small contribution from neanderthals.  We know that modern-day Europeans are not simply Paleolithic mammoth eaters who reluctantly settled down and began farming. 

OK, so Europeans are a mix of early agriculturalist and local hunter-gatherer genes, including neanderthals and perhaps other non-human hominids.  What fraction of the collective European genome derives from each?  This is where the evidence gets contentious.  Early studies indicated overall that European ancestry derives primarily from local hunter-gatherers that had been in Europe for thousands of years before the domestication of plants (1, 2, 3).  However, recent studies with more sophisticated methods, and larger sample sizes of modern and ancient genomes seem to be painting a different picture.  Here are a couple of quotes from a recent paper on mitochondrial DNA (4):

The observed changes over time suggest that the spread of agriculture in Europe involved the expansion of farming populations into Europe followed by the eventual assimilation of resident hunter-gatherers.

The [mitochondrial DNA] data thus suggest that the pre-Neolithic populations in Europe were largely replaced by in-coming Neolithic farming groups, with a maximum [mitochondrial DNA] contribution of around 20% from pre-Neolithic hunter-gatherers.

This paper has been criticized by people more knowledgeable about genetic anthropology than myself (5).  However, different methods, including approaches based on skull morphology rather than genetics, have yielded similar results (6).  Here's a paper from 2010 on the Y chromosome (7):

Taken with evidence on the origins of other haplogroups, this indicates that most European Y chromosomes originate in the Neolithic expansion. This reinterpretation makes Europe a prime example of how technological and cultural change is linked with the expansion of a Y-chromosomal lineage ...

The genetic contribution from Middle Eastern agriculturalists may decrease as one moves Northwest throughout Europe, and thus further from the Middle East.  A brand new paper attempted to estimate the proportion of the genome that derives from incoming Neolithic farmers in different European populations (8).  In the following image from the paper, the proportion of the genome derived from Neolithic farmers in different modern European populations is represented in red:


This is the authors' best guess, based on a very limited number of ancient Paleolithic and Neolithic DNA samples from archaeological sites.  The picture will certainly change as more data come in.  However, I think it illustrates the overall points clearly that a) modern Europeans are a genetic mix of indigenous Paleolithic and incoming Neolithic farmer populations, and b) the proportion of Neolithic genes generally decreases with increasing distance from the Middle East.

The story of human evolution is a story of population expansions that displace and assimilate surrounding populations.  For example, humans expanded and replaced the non-human hominids neanderthals and denisovans in Europe and Asia (although some human populations also assimilated a portion of their genome into our own, so they aren't genetically extinct).  Europeans expanded into North America and Australia, and today represent the majority of the human genetic material on those continents.  Han Chinese expanded and assimilated surrounding populations in China, and continue to do so today.  African Bantu expanded and assimilated surrounding cultures in a large swath of Africa.  There is some evidence for similar events occurring in Native American history before the arrival of Europeans.  This is due in large part to cultural and genetic adaptations that favor the expansion of certain populations.  Like it or not, this is the story of human evolution, and this expansion/assimilation scenario is a plausible explanation for what happened in ancient Europe when agriculturalists arrived. 

Do the Proportions Even Matter for Our Purposes?

The issue of how much modern European DNA comes from local hunter-gatherers, and how much comes from Middle Eastern agriculturalists, is still hotly debated, and I won't pretend to be an authority on the matter.  It will certainly vary by population.  However, I'm going to argue that for our purposes, it doesn't even matter, because the majority of modern Europeans probably carry the most important genetic adaptations to agriculture regardless of the proportion of our genome that has Middle Eastern agriculturalist ancestry.  Why?  Natural selection.  If there has been a significant amount of early agriculturalist genetic material in the European gene pool for thousands of years, which we know at a minimum to be the case, even if that amount is relatively small, natural selection would have favored the propagation of the specific genes that increase reproductive success in an agricultural environment.

Take the example of lactase persistence, a genetic mutation that allows adults to digest the milk sugar lactose.  The mutation that's most common in Europeans arose in a single individual about 7,500 years ago, shortly after the introduction of dairying, and today is present in 590 million Europeans (80 percent).

Here's a hypothetical example to illustrate the point.  You have a group of 90 hunter-gatherers eating large game in Europe 5,000 years ago.  10 Middle Eastern agriculturalists who have been farming for the last 5,000 years come along, teach the hunter-gatherers how to farm, and have children with them.  This newly agricultural population is now 90 percent hunter-gatherer, and 10 percent agriculturalist, genetically speaking.  We know that early adopters of agriculture had serious health problems that must have exerted major selective pressures on them, favoring genetic adaptations over time.  The offspring from this hybrid hunter-gatherer-agriculturalist population would be subject to the same damaging effects of the agricultural diet and lifestyle.  Over time, if the agriculturalists carried any significant genetic adaptations to an agricultural diet and lifestyle, these would be favored by natural selection and increase in frequency, just like lactase persistence.  Fast forward 5,000 years, and you could end up with a hypothetical population that's overall 88 percent descended from European hunter-gatherers, 12 percent descended from Middle Eastern agriculturalists, but nevertheless carries all the key genetic adaptations to an agricultural diet and lifestyle that the early agriculturalists brought along with them when they immigrated to Europe, not to mention any new ones they acquired in the meantime.

In the next post, I'll explain that this process of rapid genetic adaptation is not only plausible, it has already been convincingly demonstrated in humans.