welcoming in 2010!

so, 2010 starts a whole new chapter in our lives. as you know, we have officially moved...but what you may not know is that we have moved to a new town. we now live in beaufort, sc (kind of a mini charleston about 60 miles away)....and we are going to add a new addition to our family in june....a little boy (which has been another reason i have slacked in blogging...thank goodness the first trimester is over)! we are super excited about starting this new chapter and hope y'all will be around to watch it all unfold....have a wonder new years and i'll see you in 2010 :)

xoxo pink wallpaper

*i promise to be back to my old blogging ways next week and if anyone is interested in design services in beaufort or nearby, please email me!

The Body Fat Setpoint

One pound of human fat contains about 3,500 calories. That represents roughly 40 slices of toast. So if you were to eat one extra slice of toast every day, you would gain just under a pound of fat per month. Conversely, if you were to eat one fewer slice per day, you'd lose a pound a month. Right? Not quite.

How is it that most peoples' body fat mass stays relatively stable over long periods of time, when an imbalance of as little as 5% of calories should lead to rapid changes in weight? Is it because we do complicated calculations in our heads every day, factoring in basal metabolic rate and exercise, to make sure our energy intake precisely matches expenditure? Of course not. We're gifted with a sophisticated system of hormones and brain regions that do the "calculations" for us unconsciously*.

When it's working properly, this system precisely matches energy intake to expenditure, ensuring a stable and healthy fat mass. It does this by controlling food seeking behaviors, feelings of fullness and even energy expenditure by heat production and physical movements. If you eat a little bit more than usual at a meal, a properly functioning system will say "let's eat a little bit less next time, and perhaps also burn some of it off." This is one reason why animals in their natural habitat are nearly always at an appropriate weight, barring starvation. The only time wild animals are overweight enough to significantly compromise physical performance is when it serves an important purpose, such as preparing for hibernation.

I recently came across a classic study that illustrates these principles nicely in humans, titled "Metabolic Response to Experimental Overfeeding in Lean and Overweight Healthy Volunteers", by Dr. Erik O. Diaz and colleagues (1). They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume, under controlled conditions where the investigators could be confident of food intake. Macronutrient composition was 12-42-46 % protein-fat-carbohydrate.

After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass. Consistent with what one would expect if the body were trying to burn off excess calories and return to baseline fat mass, the metabolic rate and body heat production of the subjects increased.

Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%). Here is a graph showing changes in fat mass for each individual that completed the study:

We don't know if they would have lost the remaining fat mass in the following weeks because they were only followed for 6 weeks after overfeeding, although it did appear that they were reaching a plateau slightly above their original body weight. Thus, nearly all subjects "defended" their original body fat mass irrespective of their starting point. Underfeeding studies have shown the same phenomenon: whether lean or overweight, people tend to return to their original fat mass after underfeeding is over. Again, this supports the idea that the body has a body fat mass "set point" that it attempts to defend against changes in either direction. It's one of many systems in the body that attempt to maintain homeostasis.

OK, so why do we care?

We care because this has some very important implications for human obesity. With such a system in place to keep body fat mass in a narrow range, a major departure from that range implies that the system isn't functioning correctly. In other words, obesity has to involve a defect in the system that regulates body fat, because a properly functioning system would not have allowed that degree of fat gain in the first place.

So yes, we are overweight because we eat too many calories relative to energy expended. But why are we eating too many calories? There are a number of reasons, but one reason is that the system that should be defending a low fat mass is now defending a high fat mass. Therefore, the ideal solution is not simply to restrict calories, or burn more calories through exercise, but to try to work with the system that decides what fat mass to 'defend'. Restricting calories isn't necessarily a good solution because the body will attempt to defend its setpoint, whether high or low, by increasing hunger and decreasing its metabolic rate. That's why low-calorie diets, and most diets in general, typically fail in the long term. Restricting calories works for fat loss, but most people find it miserable to fight hunger every day.

This raises two questions:

1. What caused the system to defend a high fat mass?
2. Is it possible to modify the fat mass setpoint, and how would one go about it?

Given the fact that body fat mass is much higher in many affluent nations than it has ever been in human history, the increase must be due to factors that have changed in modern times. I can only speculate what these factors may be, because research has not identified them to my knowledge, at least not in humans. But I have my guesses. I'll expand on this in the next post.


* The hormone leptin and the hypothalamus are the ringleaders, although there are many other elements involved, such as several gut-derived peptides, insulin, and a number of other brain regions.

Mendeley: the reference management software

Yesterday, a friend of mine Dmitry Konstantinov told me about Mendeley. His problem was he had got a lot of papers within his computer and needed to handle them efficiently. After digging the Internet, he found Mendeley reference management system. The system allows you to sort papers, extract the title, abstract, authors, and references from textual PDFs, automatically retrieve meta-information about them from services like CiteSeer^x, annotate papers and even their paragraphs, tag papers, flag them as read/favourite etc. Full text search across all your library is very convenient too.

The project is based in London, and share some management with Last.fm. Unsurprisingly, they have a social network upon all that. You can share you paper collections, upload your articles, synchronize your library with Mendeley Web. A user has up to 500 Mb space on servers. Now I see, where the idea of SciPeople, Russian scientific network, comes from. I don't know if such networks are the future of science, but they are, however, worth paying attention.

My profile.

Science vs. Industry

Yesterday I was called by an HR officer from NetCracker, my former employer. She told me they "have a lot of new activities", so now they "fulfil repeated recruiting" and suggested to return to NetCracker. It is really funny, because 1.5 years ago they told me that according to the corporate policy it was impossible to employ somebody who had left the company once. I politely rejected them, but the talk refreshed my memories about previous hesitations.

When I switched the company to Graphics & Media Lab, it was a hard decision. That time I firmly decided to prefer scientific career over industrial. I considered a lot of pros and cons to make the decision. Although they are often personal, I'd like to share my observations with you.

Advantages of research work:

• When you work as a researcher, you invent something new instead of just coding different stuff. This job is creative, not just constructive.
• When you work as a programmer, you result is just a code. You don't publish papers, no one knows about your results. Moreover, they are often proprietorial.
• If you work as an office worker or a manager, you could be paid a lot of money, but you are supposed to work 24x7. It really sucks because you do really annoying paperwork or participate in meetings, but do not produce anything substantial. If you have a lot of money, you have no time or desire to spend them to anything interesting. That's the reason why my roommate Andrey Korolev left Shell.
• When you work as a scientist, you should not learn all the boring technologies. You can't be a prominent Java programmer without knowing heaps of jXxx libraries, a number of frameworks and without having some useless certificates. Besides, your knowledge could be narrow, they are restricted by your employer's needs.
• Scientists are mobile: they move from one university to another. Some universities do not prolong contracts with professors, even if they are very cool. For me, it seems boring to live all the life in one place. (Though you could be sent to business trips while you work at some big corporation)
• If you work at university, you might have a teaching experience of some kind, which is useful for you, if you use it properly.

Advantages of industrial work:

• The main advantage is a good salary. :) If you are not a complete geek, it does matter. Science is usually funded by grants, which is unstable.
• Since your employer needs profit, you do something practical. You can be sure that you don't investigate some abstract stuff that will never be applied.

Trust or not, our lab combines advantages of both directions. We usually work on projects ordered by customers who pay for it. Of course, we select only those projects, in which we can get some scientific results. Actually, it is done automatically, because it is not profitable for a customer to pay us for coding. That's how applied science should work, I think.

Rabbits on a High-Saturated Fat Diet Without Added Cholesterol

I just saw another study that supports my previous post Animal Models of Atherosclerosis: LDL. The hypothesis is that in the absence of excessive added dietary cholesterol, saturated fat does not influence LDL or atherosclerosis in animal models, relative to other fats (although omega-6 polyunsaturated oils do lower LDL in some animal models). This appears to be consistent with what we see in humans.

In this study, they fed four groups of rabbits different diets:

1. Regular low-fat rabbit chow
2. Regular low-fat rabbit chow plus 0.5 g cholesterol per day
3. High-fat diet with 30% calories as coconut oil (saturated) and no added cholesterol
4. High-fat diet with 30% calories as sunflower oil (polyunsaturated) and no added cholesterol

LDL at 6 months was the same in groups 1, 3 and 4, but was increased more than 20-fold in group 2. It's not the fat, it's the fact that they're overloading herbivores with dietary cholesterol!

Total cholesterol was also the same between all groups except the cholesterol-fed group. TBARS, a measure of lipid oxidation in the blood, was elevated in the cholesterol and sunflower oil groups but not in the chow or coconut groups. Oxidation of blood lipids is one of the major factors in atherosclerosis, the vascular disease that narrows arteries and increases the risk of having a heart attack. Serum vitamin C was lower in the cholesterol-fed groups but not the others.

This supports the idea that saturated fat in the absence of excess dietary cholesterol does not necessarily increase LDL, and in fact in most animals it does not.

Merry Christmas!

Hello, world!

Well, I've just started my technical/research blog.

Why?

I already have a personal blog, which is (I hope) used to be read by a number of my friends. In recent time I noticed that I had begun post a lot of technical stuff my friends were not interested in. Also, that blog is in Russian, which limits its audience. So, I preferred not to change the blog policy but create a new blog. It was also Boris Yangel's amazing blog that inspired me to create mine.

Computer blindness?

Well, yes. Folks who know me might already divine that the blog is primarily about computer vision, and they are certainly right. I chose such a fancy name because computer vision is somewhat disappointing. Let me explain.

Do you remember that story when Marvin Minsky at MIT asked his student to teach a computer understand the scene retrieved from a camera during the 1966 summer break? Unsurprisingly, the student failed. Moreover, the general task is far from being solved even now. That days computers were slow, and AI scientists thought that performing logical inference is way more complicated than just scene analysis. Now, we have Prolog and a pile of different verification systems (thanks to the university curriculum -- we used some of them), but a computer is not able to recognize even simple object categories on different classes of images (e.g. relatively robust face detection was done only in early 2000s by Viola and Jones).

Actually, not only Minsky was misled. If you are a vision researcher, when you tell people about your research, they are likely to reply: "Is that all you can? Man, it's simple!" Sure, it is simple for you to figure out that it is a cow on the meadow, not a horse, but try to explain it to computer! It is actually a problem in our lab: when vision guys try to defend a Masters/PhD thesis in front of the committee (which consists of folks who do research in computer hardware, system programming etc), and the committee is usually not impressed by the results, because they think it is not too difficult.

Okay, you've got the point. Computers are blind, and we should cope with that.

Next. Do you know, what's the difference between computer vision of 1980s and modern computer vision? In 80s, they used to solve particular problems, not general ones. They could implement quite a decent vision system that performed its task, but it could not be transferred to another domain. Nowadays, such approach is no more scientific, while it is still good for engineers. Today, computer vision science is about general tasks. It became possible because of extensive using of machine learning methods (a lot of them were developed in '90s). Vision is nothing without learning now. I hope you've got this point too: Vision + Learning = Forever Together. That's why my blog cannot ignore machine learning issues.

What else? Programming language is a tool, but it can be interesting per se. I am about to finish a 5-year university programme in Computer Science, so I have been being taught different language concepts and programming paradigms, and I find it interesting sometimes. That is another possible topic.

Finally,

Subscribe me, read me and comment me. Everybody is welcome! Let it roll!

It's all in the training

Merry Christmas and Happy New Year

Tomat Alternatif Pengganti Aspirin
By Republika Newsroom
Rabu, 23 Desember 2009 pukul 11:40:00




LONDON--Kandungan gel atau gelatin alami yang terdapat dalam tomat telah diidentifikasi peneliti di Inggris sebagai kunci penting untuk kesehatan. Gel ini diyakini para peneliti mampu melancarkan sirkulasi darah.

Secara karakteristik, gel pada tomat umumnya berwarna dan memiliki rasa. Peneliti di Inggris bahkan meyakini bahwa gel itu bila dibaurkan pada makanan tidak akan mengubah komponen dasarnya.

Komisi Kesehatan Uni Eropa yang telah menerima laporan dari peneliti asal Inggris terkait kandungan pada gel tomat yang mampu memperlancar peredaran darah, telah menyetujui Penggunaan getah ini dalam bentuk obat kemasan.

Sementara itu, jutaan masyarakat berusia lanjut telah mengkonsumsi aspirin dalam dosis rendah guna memperlancar peredaran darah. Meski begitu, peneliti merasa khawatir penggunaan aspirin meninggalkan efek seperti pendarahan pada perut dan pembentukan bisul.

Profesor Asim Dutta-Roy dari Rowwet Institute di Aberdeen, Skotlandia mengatakan Fruitflow (nama gel tomat itu)sangat baik untuk digunakan sebagai pengganti aspirin.

"Hingga kini, tidak terlihat efek negatif yang berhasil terekam saat percobaan pengembangan Fruitflow berlangsung," tukasnya seperti dilansir Telegraph, Rabu (23/12).

Pernyataan Dutta-Roy juga didukung keberhasilan fruitflow memberikan efek terhadap peredaraan darah hanya 3 jam setelah dikonsumsi dan manfaatnya pada tubuh berlangsung hingga 18 Jam. Hasil ini tentu ideal untuk dikonsumsi setiap hari.

Dalam perkembangannya, fruitflow tidak hanya dikonsumsi dalam bentuk tablet atau kapsul tapi juga jus. Fruitflow sendiri sudah dijual bebas diberbagai apotik atau toko obat. cr2/rin

What's the Ideal Fasting Insulin Level?

[2013 update.  I'm leaving this post up for informational purposes, but I think it's difficult to determine the "ideal" insulin level because it depends on a variety of factors including diet composition.  Also, insulin assays are not always comparable to one another, particularly the older assays, so it's difficult to compare between studies]

Insulin is an important hormone. Its canonical function is to signal cells to absorb glucose from the bloodstream, but it has many other effects. Chronically elevated insulin is a marker of metabolic dysfunction, and typically accompanies high fat mass, poor glucose tolerance (prediabetes) and blood lipid abnormalities. Measuring insulin first thing in the morning, before eating a meal, reflects fasting insulin. High fasting insulin is a marker of metabolic problems and may contribute to some of them as well.

Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL.

Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.

In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.

Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).

I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:

1. It's hard to be sure that they didn't eat anything prior to the blood draw.
2. From what I understand, insulin assays were variable and not standardized back then.
3. In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.

Now you know the conflicting evidence, so you're free to be skeptical if you'd like.

We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. This is despite a substantial intake of carbohydrate, including fruit and vegetable sugars.  The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).

One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, and a relatively healthy diet growing up. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction.

So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template.

ho ho ho.

SERIOUSLY- 4 days until a chubby little man in a red suit comes down your chimney....are you ready?!!

me? ha- not so much...but who cares, its our first christmas in this house and we are going to make the most of it. usually we are traveling to see my parents and warren's but this year everyone is coming to us...can you hear the excitement in my typing for not having to travel this year?!! which means, i should really be cleaning (not my best forte) instead of typing...but i couldn't resist saying hello!! oh and i have internet again- YIPPEE!! so watch out :)

*images courtesy of martha stewart

Swimming now part of our training for Medway

• Minus 5 degrees
• A frozen creek
• A dozen trail runners ready to cross via rocks and tree limbs
• One runner wants to show how to run across the ice
• He now finds out that ice can be slippery
• His feet fly up & lands on his back and breaks the ice
• That sinking feeling
• He is OK but soaked
• PRICELESS
  

The Dirty Little Secret of the Diet-Heart Hypothesis

The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. What have these studies found?

The large majority of observational studies have found no connection between habitualsaturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.

A Sampling of Unsupportive Studies

Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:

A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.

Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.

Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.

Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.

Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.

Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.

Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.

Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.

Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. The abstract claims that saturated fat was associated with heart attack risk. However, the association disappeared when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.

Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.

I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is a dominant cause of cardiovascular disease, why are its effects essentially undetectable in the best studies we can muster?

Studies that Support the Diet-Heart Hypothesis

To be complete, some studies have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:

Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was very small.

Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."

Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.

The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.

The Review Papers

Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. In case you're concerned that I'm cherry-picking studies, here are links to review papers on the same data that have reached the same conclusion:

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.  American Journal of Clinical Nutrition. 2010.  "A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD."

A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association between saturated fat consumption and heart attack risk.

The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov challenges the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.

Where's the Disconnect?

The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?

There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol.

So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. Could this hypothesis be less well supported than it appears?  The data that are used to support it come almost exclusively from short-term feeding studies (<3 and="" association="" between="" blood="" consumption="" effect="" fat="" found="" habitual="" have="" here="" how="" information="" is="" lipids.="" little="" long="" months="" most="" nbsp="" observational="" on="" p="" persists="" saturated="" studies="" surprisingly="" this="">

Sepotong "Tempe" Bisa Mencegah Kanker
Selain kanker, tempe juga bisa mengurangi risiko terjadinya penyakit gagal ginjal.
Senin, 14 Desember 2009, 09:54 WIB
Amril Amarullah


SURABAYA POST -- Dikenal sebagai makanan rakyat kecil, tempe ternyata memiliki khasiat menanggulangi berbagai macam penyakit. Menurut ahli teknologi pangan dan gizi, Prof Made Astawan, banyak mengonsumsi tempe bisa mengurangi risiko terkena penyakit kanker.

Selain kanker, tempe juga bisa mengurangi risiko terjadinya penyakit gagal ginjal, osteoporosis atau keropos tulang, dan diabetes mellitus atau kencing manis. Tempe bisa mencegah kanker, untuk pria bisa mencegah kanker prostat dan para perempuan bisa mencegah kanker payudara," kata Prof Made

Dijelaskan, bakan baku tempe berupa kedelai itu memiliki kandungan gizi yang tinggi. Di antara jenis kacang-kacangan, kedelai merupakan jenis yang paling bagus. Karenanya kedelai mendapatkan julukan.

Dan sepotong tempe membutuhkan kedelai yang jumlahnya sangat banyak. "Dalam sebutir kedelai ada kandungan gizi dan non gizi yang sangat dibutuhkan manusia,"ungkap Wakil Ketua Forum Tempe Indonesia itu.

Ditambahkan, kandungan gizi dalam kedelai di antaranya protein nabatinya yang tergolong paling bagus. Selain protein nabati, kedelai juga mengandung asam amino esensial lengkap sehingga mudah dicerna dan diserap oleh tubuh.

Sedang kandungan lemak nabatinya mengandung Omega 3 dan Omega 6 yang sangat dibutuhkan oleh tubuh. Kedelai juga mengandung vitamin B-12. Selain kandungan gizi, ungkap Made, kandungan non gizi kedelai juga sangat bagus.

Setiap butir kedelai mengandung serat pangan yang sangat baik untuk kesehatan usus. Sehingga bisa mencegah terjadinya berbagai penyakit di usus, bahkan kanker usus. Tak hanya serat pangan, kedelai juga mengandung senyawa-senyawa vitokimia. Senyawa ini mengandung isoflavon yang berfungi sebagai antioksidan.

Pada bayi dan anak-anak bisa mencegah terjadinya diare, pada pria bisa mencegah penyakit kanker prostat, sedang pada wanita bisa mencegah penyakit kanker payudara dan sangat bagus dikonsumsi menjelang menopause. Isoflavonjuga baik untuk mencegah gagal ginjal, kencing manis, dan osteoporosis, dan diabetes.

Laporan: Siska Prestiwati
• VIVAnews

Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance?

An Interesting Finding

Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:

The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.

Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:

Butyrate and its derivatives may have potential application in the prevention and treatment of metabolic syndrome in humans.

There's one caveat, however: the butyrate group at less food. Something about the butyrate treatment caused their food intake to decline after 3 weeks, dropping roughly 20% by 10 weeks. The investigators cleverly tried to hide this by normalizing food intake to body weight, making it look like the food intake of the comparison group was dropping as well (when actually it was staying the same as this group was gaining weight).  This does cast some doubt on the health-promoting effects of high-dose butyrate.

I found this study thought-provoking, so I looked into butyrate further.

Butyrate Suppresses Inflammation in the Gut and Other Tissues

In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.

It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Some investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.

Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal permeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).

Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.

Butyrate Increases Resistance to Metabolic and Physical Stress

Certain types of fiber reduce atherosclerosis in animal models, and this effect may be due to butyrate production produced when the fiber is fermented. Fiber intake was associated with lower blood markers of inflammation in the Women's Health Initiative study, and has been repeatedly associated with lower heart attack risk and reduced progression of atherosclerosis in humans. Butyrate also sharply reduces the harmful effects of type 1 diabetes in rats, as does dietary fiber to a lesser extent.

Butyrate increases the function and survival of mice with certain neurodegenerative diseases. Polyglutamine diseases, which are the most common class of genetic neurodegenerative diseases, are delayed in mice treated with butyrate (1, 2, 3). Many of you have probably heard of Huntington's disease, which is the most common of the class. I did my thesis on a polyglutamine disease called SCA7, and this is the first suggestion I've seen that diet may be able to modify its course.

Yet another interesting finding in the first paper I discussed: mice treated with butyrate were more cold-resistant than the comparison group. When they were both placed in a cold room, body temperature dropped quite a bit in the comparison group, while it remained relatively stable in the butyrate group, despite the fact that the butyrate group was leaner****. This was due to increased heat production in the butyrate group.

Due to the potent effect butyrate has on a number of bodily processes, it may be a fundamental controller of metabolism, stress resistance and the immune system in mammals.

An Ancient Line of Communication Between Symbiotic Organisms

Why does butyrate have so much control over inflammation? Let's think about where it comes from. Bacteria in the gut produce it. It's a source of energy, so our bodies take it up readily. It's one of the main molecules that passes from the symbiotic (helpful) bacteria in the gut to the rest of the body. Could it be that the body receives butyrate as a signal that there's a thriving colony of symbiotic bacteria in the gut, inducing immune tolerance to them? The body may alter its immune response (inflammation) in order to permit a mutually beneficial relationship between itself and its symbionts.

Sources of Butyrate

There are two main ways to get butyrate and other short-chain fatty acids. The first is to eat fiber and let your intestinal bacteria do the rest. Whole plant foods such as sweet potatoes, properly prepared whole grains, beans, vegetables, fruit and nuts are good sources of fiber. Refined foods such as white flour, white rice and sugar are very low in fiber. Clinical trials have shown that increasing dietary fiber increases butyrate production, and decreasing fiber decreases it (free full text).

Butyrate also occurs in significant amounts in food. What foods contain butyrate? Hmm, I wonder where the name BUTYR-ate came from? Butter perhaps? Butter is 3-4 percent butyrate, the richest known source. But everyone knows butter is bad for you, right?

After thinking about it, I've decided that butyrate may have been a principal component of Dr. Weston Price's legendary butter oil. Price used this oil in conjunction with high-vitamin cod liver oil to heal tooth decay and a number of other ailments in his patients. The method he used to produce it would have concentrated fats with a low melting temperature, including butyrate, in addition to vitamin K2*****. Thus, the combination of high-vitamin cod liver oil and butter oil would have provided a potent cocktail of fat-soluble vitamins (A, D3, K2), omega-3 fatty acids and butyrate. It's no wonder it was so effective in his patients.


* According to insulin tolerance test.

** Acetate (acetic acid, the main acid in vinegar), propionate and butyrate are the primary three fatty acids produced by intestinal fermentation.

*** The lowest concentration used in this study, 30 micromolar, is probably higher than the concentration in peripheral serum under normal circumstances. Human serum butyrate is in the range of 4 micromolar in British adults, and 29 micromolar in the hepatic portal vein which brings fats from the digestive tract to the liver (ref). This would likely be at least two-fold higher in populations eating high-fiber diets.

**** Due to higher mitochondrial density in brown fat and more mitochondrial uncoupling.

***** Slow crystallization, which selectively concentrates triglycerides with a low melting point.

*Poof*

dear fairy godmother,

please magically come and unpack all of my boxes, explain to my poor readers- if i have any left- why i have been gone so long (not having access to the internet is a real you-know-what), help taylor realize that she doesn't need to wake up at 4:30 AM to tell me to read her a book, and lastly- make me not envious of this beautifully decorated/ perfection of a house.....oh, and is it too much to ask to throw in that part about: and they all lived happily ever after (i could really use that right about now)??!

thanks bunches-

pink wallpaper

*images courtesy of daisy chain, one kings lane

Manfat Meniran utk Penderita GAGAL GINJAL

Berikut cuplikan artikel tentang Manfat Meniran utk Penderita GAGAL GINJAL semoga bermanfaat. :

Untuk meniran, sebenarnya ada 2 tanaman yaitu species Phyllantus niruri dan Phyllanthus urinaria . Saya jelaskan tentang perbedaan kedua meniran di atas. Secara umum perbedaan antara P. niruri dan P. urinaria terletak pada warna batangnya. P. niruri memiliki batangnya berwarna putih sedangkan P. urinaria batangnya berwarna merah.
Keduanya memang mempunyai sifat diuresis yaitu sifat mengeluarakan air kencing, dan tentu proses ini berhubungan erat dengan kerja ginjal. Ya memang demikian, sebelum di-klaim sebagai imunomodulator meniran telah dikenal sebagai obat yang bikin kencing.
Bagaimana dengan sifat diuresis tersebut? Pada dosis tertentu ternyata mempunyai efek imunostimulan, (baca artikel: Stimuno Untuk Kekebalan Tubuh) dan pada kadar tertentu juga bersifat diuresis. Si batang merah ini sifat diuresisnya lebih kuat dibanding P. niruri. Bagaimana dengan penderita ginjal?

Berikut komentar bapak Didik Gunawa, Dosen Farmasi UGM:

“Sebagai penderita gagal ginjal, kemampuan tubuh untuk pembentukan Hb terhenti, sehingga kadar Hb saya setiap waktu cenderung turun dan tiap 6 bulan sekali butuh transfusi darah.
Dari berbagai hasil penelitian dilaporkan bahwa herba meniran (Phyllanthus niruri) memiliki kemampuan meningkatkan kadar Hb dalam darah, dan setelah saya coba mengkonsumsi infusa herba meniran dalam waktu 2 bulan, ternyata potensi itu memang terbukti bisa meningkatkan kadar Hb dalam darah.

Dari hasil penelitian pula dilaporkan bahwa meniran berfungsi membantu aktivitas kerja hormon pembentuk Hb (alfa atau beta Haemapoeitin : yang hormon ini tidak lagi diproduksi oleh ginjal yang rusak). Sejak itu selama 2 tahun terakhir, saya tidak lagi pernah transfusi darah, dan Hb saya stabil antara 8,5 – 9,5 (kadar normal orang sehat = 12).Transfusi disarankan kalau kadar Hb turun sampai 7 ke bawah.

Semoga informasi ini bisa dimanfaatkan para penderita gagal ginjal yang lain. “



Artikel ini ditulis berasal dari disuksi dengan saudara Puguh Novi Arsito, seorang sarjani farmasi dari minat Farmasi Bahan Alam. Ini adalah pertama kalinya, UGM meluluskan sarjana farmasi minat bahan alam, untuk bertugas mengolah kekayaan hayati berkhasiat obat yang ada di Indonesia (misi fakultas).
Oleh: Sarmoko (minat Farmasi Sains dan Industri).
http://moko31.wordpress.com/2009/05/01/jamu-obat-herbal-terstandar-oht-dan-fitofarmaka/


NB: Jika memerlukan Extract Meniran, hrga 75rb/50 kpsul silahkan contact sy budiprakoso98@gmail.com atau 081310343598

Malocclusion: Disease of Civilization, Part IX

A Summary

For those who didn't want to wade through the entire nerd safari, I offer a simple summary.

Our ancestors had straight teeth, and their wisdom teeth came in without any problem. The same continues to be true of a few non-industrial cultures today, but it's becoming rare. Wild animals also rarely suffer from orthodontic problems.

Today, the majority of people in the US and other affluent nations have some type of malocclusion, whether it's crooked teeth, overbite, open bite or a number of other possibilities.

There are three main factors that I believe contribute to malocclusion in modern societies:

1. Maternal nutrition during the first trimester of pregnancy. Vitamin K2, found in organs, pastured dairy and eggs, is particularly important. We may also make small amounts from the K1 found in green vegetables.
2. Sucking habits from birth to age four. Breast feeding protects against malocclusion. Bottle feeding, pacifiers and finger sucking probably increase the risk of malocclusion. Cup feeding and orthodontic pacifiers are probably acceptable alternatives.
3. Food toughness. The jaws probably require stress from tough food to develop correctly. This can contribute to the widening of the dental arch until roughly age 17. Beef jerky, raw vegetables, raw fruit, tough cuts of meat and nuts are all good ways to exercise the jaws.
   

And now, an example from the dental literature to motivate you. In 1976, Dr. H. L. Eirew published an interesting paper in the British Dental Journal. He took two 12-year old identical twins, with identical class I malocclusions (crowded incisors), and gave them two different orthodontic treatments. Here's a picture of both girls before the treatment:


In one, he made more space in her jaws by extracting teeth. In the other, he put in an apparatus that broadened her dental arch, which roughly mimics the natural process of arch growth during childhood and adolescence. This had profound effects on the girls' subsequent occlusion and facial structure:

The girl on the left had teeth extracted, while the girl on the right had her arch broadened. Under ideal circumstances, this is what should happen naturally during development. Notice any differences?

Thanks to the Weston A Price foundation's recent newsletter for the study reference.