Warung Bebas

Senin, 20 Desember 2010

"You only got in because you are a [woman, person of color, person with disabilities]"

I recently stumbled across a fantastic blog called "What Is It Like To Be A Woman In Philosophy". Philosophy probably has more underrepresentation than CS does, or maybe we're tied, I'm not sure. In any case, this blog is set up in such a way that women in Philosophy submit anecdotes which get posted anonymously.

Today I read this post, and the lines at the end really struck a chord:
"As one of the only female graduate students, I was very involved in a recent job search in which the only fly outs were women. After the final job talk I was stopped in the hall and asked by a group of male faculty members what my thoughts on the candidates were. I said that I thought they all seemed equally qualified, but that candidate X was particularly friendly, approachable, and outgoing while also setting an excellent example of professionalism for the female grad studens. One senior male faculty member interrupted me midsentence with: 'Well they’re all women, so what more do you want?' This was the same faculty member who told me in my first year that I had only been accepted to the PhD program because they 'went out of their way to accept more women' that year. None of the other faculty members reproached him, they all just wandered away into their offices."
Two things about this are problematic. First, someone from a majority group telling someone from a minority group that the only reason they achieved (or can achieve) something was because they are a minority. Statements like this are extraordinarily hurtful because in addition to implying the minority person is not capable of quality, competitive work, it also says very clearly: I do not accept you, and you are not a part of my club.

Ouch.

But double ouch is this: the other faculty members did nothing. This makes me sadder than I can say. Are these faculty members so risk and conflict-averse that they don't stand up to such malarky? When my cousin-in-law made racist jokes at a New Year's Eve party last year, I immediately splashed water in her face. It's like when the cat scratches the couch and you spray them with the water bottle. Conditioning 101.

For the menfolk and other majority folks out there who want to help:  if you truly want to make your workplace hospitable for women, people of color, people with disabilities, etc, you have to help socialize the people who didn't get the memo. Pick those fights - take some risks to help out someone else. This is what it takes to help change things.

Dairy Fat and Diabetes

Introduction

Having access to embargoed news from the Annals of Internal Medicine is really fun. I get to report on important studies at the same time as the news media. But this week, I got my hands on a study that I'm not sure will be widely reported (Mozaffarian et al. Trans-palmitoleic Acid, Metabolic Risk Factors, and New-Onset Diabetes in US Adults. Ann Internal Med. 2010). Why? Because it suggests that dairy fat may protect against diabetes.

The lead author is Dr. Dariush Mozaffarian, whose meta-analysis of diet-heart controlled trials I recently criticized (1). I think this is a good opportunity for me to acknowledge that Dr. Mozaffarian and his colleagues have published some brave papers in the past that challenged conventional wisdom. For example, in a 2005 study, they found that postmenopausal women who ate the most saturated fat had the slowest rate of narrowing of their coronary arteries over time (2). It wasn't a popular finding but he has defended it. His colleague Dr. Walter Willett thinks dietary fat is fine (although he favors corn oil), whole eggs can be part of a healthy diet, and there are worse things than eating coconut from time to time. Dr. Willett is also a strong advocate of unrefined foods and home cooking, which I believe are two of the main pillars of healthy eating.

Let's hit the data


Investigators collected two measures of dairy fat intake in 3,736 Americans:
  1. 24 hour dietary recall questionnaires, six times. This records volunteers' food intake at the beginning of the study.
  2. Blood (plasma phospholipid) content of trans-palmitoleate. Dairy fat and red meat fat are virtually the only sources of this fatty acid, so it reflects the intake of these foods. Most of the trans-palmitoleate came from dairy in this study, although red meat was also a significant source.
After adjustment for confounding factors, trans-palmitoleate levels were associated with a smaller waist circumference, higher HDL cholesterol, lower serum triglycerides, lower C-reactive protein, lower fasting insulin and lower calculated insulin resistance. Furthermore, people with the highest trans-palmitoleate levels had 1/3 the risk of developing diabetes over the three years volunteers were followed. Keep in mind, however, that this is an observational study and does not prove that dairy fat prevents diabetes.

Even though certain blood fatty acids partially represent food intake, they can also represent metabolic conditions. For example, people on their way to type II diabetes tend to have more saturated blood lipids, independent of diet (3, 4)*. So it's reassuring to see that dietary trans-palmitoleate intake was closely related to the serum level. The investigators also noted that "greater whole-fat dairy consumption was associated with lower risk for diabetes," which increases my confidence that serum trans-palmitoleate is actually measuring dairy fat intake to some degree. However, in the end, I think the striking association they observed was partially due to dairy fat intake, but mostly due to metabolic factors that had nothing to do with dairy fat**.

Here's a nice quote:
Our findings support potential metabolic benefits of dairy consumption and suggest that trans-palmitoleate may mediate these effects***. They also suggest that efforts to promote exclusive consumption of low-fat and nonfat dairy products, which would lower population exposure to trans-palmitoleate, may be premature until the mediators of the health effects of dairy consumption are better established.
Never thought I'd see the day! Not bad, but I can do better:
Our findings support eating as much butter as possible****. Don't waste your money on low-fat cream, either (half-n-half). We're sorry that public health authorities have spent 30 years telling you to eat low-fat dairy when most studies are actually more consistent with the idea that dairy fat reduces the risk obesity and chronic disease.
What are these studies suggesting that dairy fat may be protective, you ask? That will be the topic of another post, my friends.


*Probably due to uncontrolled de novo lipogenesis because of insulin resistance. Many studies find that serum saturated fatty acids are higher in those with metabolic dysfunction, independent of diet. They sometimes interpret that as showing that people are lying about their diet, rather than that serum saturated fatty acids don't reflect diet very well. For example, in one study I cited, investigators found no relationship between dietary saturated fat and diabetes risk, but they did find a relationship between serum saturated fatty acids and diabetes risk (5). They then proceeded to refer to the serum measurements as "objective measurements" that can tease apart "important associations with diabetes incidence that may be missed when assessed by [food questionnaires]." They go on to say that serum fatty acids are "useful as biomarkers for fatty acid intake," which is true for some fatty acids but not remotely for most of the saturated ones, according to their own study. Basically, they try to insinuate that dietary saturated fat is the culprit, and the only reason they couldn't measure that association directly is that people who went on to develop diabetes inaccurately reported their diets! A more likely explanation is that elevated serum saturated fatty acids are simply a marker of insulin resistance (and thus uncontrolled de novo lipogenesis), and had nothing to do with diet.

**Why do I say that? Because mathematically adjusting for dairy and meat fat intake did not substantially weaken the association between phospholipid trans-palmitoleate and reduced diabetes risk (Table 4). In other words, if you believe their math, dairy/meat fat intake only accounted for a small part of the protective association. That implies that healthy people maintain a higher serum phospholipid trans-palmitoleate level than unhealthy people, even if both groups eat the same amount of trans-palmitoleate. If they hadn't mentioned that full-fat dairy fat intake was directly associated with a lower risk of diabetes, I would not find the study very interesting because I'd have my doubts that it was relevant to diet.

***I find it highly doubtful that trans-palmitoleate entirely mediates the positive health outcomes associated with dairy fat intake. I think it's more likely to simply be a marker of milk fat, which contains a number of potentially protective substances such as CLA, vitamin K2, butyric acid, and the natural trans fats including trans-palmitoleate. In addition, dairy fat is low in omega-6 polyunsaturated fat. I find it unlikely that their fancy math was able to tease those factors apart, because those substances all travel together in dairy fat. trans-palmitoleate pills are not going to replace butter.

****That's a joke. I think butter can be part of healthy diet, but that doesn't mean gorging on it is a good idea. This study does not prove that dairy fat prevents diabetes, it simply suggests that it may.

Minggu, 19 Desember 2010

Potato Diet Interpretation

If you read my post on December 16th, you know that Chris Voigt saw remarkable fat loss and improvements in health markers as a result of two months of eating almost nothing but potatoes. This has left many people scratching their heads, because potatoes are not generally viewed as a healthy food. This is partially due to the fact that potatoes are very rich in carbohydrate, which also happens to be a quickly digested type, resulting in a high glycemic index. The glycemic index refers to the degree to which a particular food increases blood glucose when it's eaten, and I've questioned the relevance of this concept to health outcomes in the past (1, 2, 3). I think Mr. Voigt's results once again argue against the importance of the glycemic index as a diet-health concept.

It's often pointed out that potatoes are low in vitamins and minerals compared to vegetables on a per-calorie basis, but I think it's a misleading comparison because potatoes are much more calorie-dense than most vegetables. Potatoes compare favorably to other starchy staples such as bread, rice and taro.

Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).

On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But of course, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.

Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?

I believe Mr. Voigt's diet lowered his fat mass 'setpoint'. In other words, for whatever reason, the diet made his body 'want' to be leaner that it already was. His body began releasing stored fat that it considered excess, and therefore he had to eat less food to complete his energy needs. You see this same phenomenon very clearly in rodent feeding studies. Changes in diet composition/quality can cause dramatic shifts in the fat mass setpoint (5, 6). Mr. Voigt's appetite would eventually have returned to normal once he had stabilized at a lower body fat mass, just as rodents do.

Rodent studies have made it clear that diet composition has a massive effect on the level of fat mass that the body will 'defend' against changes in calorie intake (5, 6). Human studies have shown similar effects from changes in diet composition/quality. For example, in controlled diet trials, low-carbohydrate dieters spontaneously reduce their calorie intake quite significantly and lose body fat, without being asked to restrict calories (7). In Dr. Staffan Lindeberg's Paleolithic diet trials, participants lost a remarkable amount of fat, yet a recent publication from his group shows that the satiety (fullness) level of the Paleolithic group was not different from a non-Paleolithic comparison group despite a considerably lower calorie intake over 12 weeks (8, 9). I'll discuss this important new paper soon. Together, this suggests that diet composition/quality can have a dominant impact on the fat mass setpoint.

One possibility is that cutting the wheat, sugar, most vegetable oil and other processed food out of Mr. Voigt's diet was responsible for the fat loss.  Many people find, for example, that they lose fat simply by eliminating wheat from their diet.

Another possibility that I've been exploring recently is that changes in palatability (pleasantness of flavor) influence the fat mass setpoint. There is evidence in rodents that it does, although it's not entirely consistent. For example, rats will become massively obese if you provide them with chocolate flavored Ensure (a meal replacement drink), but not with vanilla or strawberry Ensure (10). They will defend their elevated fat mass against calorie restriction (i.e. they show a physiological starvation response when you try to bring them down to a lower weight by feeding them less chocolate Ensure) while they're eating chocolate Ensure, but as soon as you put them back on unpurified rodent pellets, they will lose fat and defend the lower fat mass. Giving them food in liquid or paste form often causes obesity, while the same food in solid pellet form will not. Eating nothing but potatoes is obviously a diet with a low overall palatability.

So I think that both a change in diet composition/quality and a decrease in palatability probably contributed to a decrease in Mr. Voigt's fat mass setpoint, which allowed him to lose fat mass without triggering a starvation response (hunger, fatigue).

The rest of his improvements in health markers were partially due to the fat loss, including his decreased fasting glucose, decreased triglycerides, and presumably increased insulin sensitivity. They may also have been partially due to a lack of industrial food and increased intake of certain micronutrients such as magnesium.

One of the most striking changes was in his calculated LDL cholesterol ("bad" cholesterol), which decreased by 41%, putting him in a range that's more typical of healthy non-industrial cultures including hunter-gatherers. Yet hunter-gatherers didn't eat nothing but potatoes, often didn't eat much starch, and in some cases had a high intake of fat and saturated fat, so what gives? It's possible that a reduced saturated fat intake had an impact on his LDL, given the relatively short timescale of the diet. But I think there's something mysterious about this setpoint mechanism that has a much broader impact on metabolism than is generally appreciated. For example, calorie restriction in humans has a massive impact on LDL, much larger than the impact of saturated fat (11). And in any case, the latter appears to be a short-term phenomenon (12). It's just beginning to be appreciated that energy balance control systems in the brain influence cholesterol metabolism.

Mr. Voigt's digestion appeared to be just fine on his potato diet, even though he generally ate the skins. This makes me even more skeptical of the idea that potato glycoalkaloids in common potato varieties are a health concern, especially if you were to eliminate most of the glycoalkaloids by peeling.

I asked Mr. Voigt about what foods he was craving during the diet to get an idea of whether he was experiencing any major deficiencies. The fact that Mr. Voigt did not mention craving meat or other high-protein foods reinforces the fact that potatoes are a reasonable source of complete protein. The only thing he craved was crunchy/juicy food, which I'm not sure how to interpret.

He also stopped snoring during the diet, and began again immediately upon resuming his normal diet, perhaps indicating that his potato diet reduced airway inflammation. This could be due to avoiding food allergies and irritants (wheat anyone?) and also fat loss.

Overall, a very informative experiment! Enjoy your potatoes.


*Until the last 5.5 weeks, when he deliberately stuffed himself beyond his appetite because his rapid weight loss worried him. Yet, even with deliberate overfeeding up to his estimated calorie requirement of 2,200 calories per day, he continued to lose weight. He probably was not quite reaching his calorie goal, or his requirement is higher than he thought.

Sabtu, 18 Desember 2010

Trouble With RSS Feed?

I've received several comments that my blog posts are no longer showing up in peoples' RSS feeds. I've gone into my settings, and the blog is still set to full feed mode, so I don't know why that would be. I'm trying to understand if the problem is widespread or only affects a few people. Please let me know in the comments section if new posts (since the potatoes and human health series) are not showing up in your reader. Also, please let me know if new posts are showing up. Thanks!

Kamis, 16 Desember 2010

Otak Sangat Rakus akan Oksigen
Irna Gustia - detikHealth- 17/11/2010



Jakarta, Otak rentan mengalami kerusakan saat mengalami kekurangan oksigen. Maka itu perbanyaklah oksigen yang masuk ke tubuh agar kondisi otak tetap terjaga, karena kekurangan oksigen bisa mengakibatkan kecacatan hingga kematian.

Dilansir MayoClinic, Kamis (16/12/2010), otak sangat rakus akan oksigen. Meskipun komposisi otak hanya 2 persen dari total massa tubuh, bagian ini menghabiskan total 20 persen kebutuhan oksigen. Artinya, seperlima dari suplai oksigen yang masuk saat bernapas akan langsung lari ke otak.

Begitu besarnya kebutuhan otak akan oksigen sementara otak hanya memiliki sedikit oksigen cadangan. Hal ini juga yang menyebabkan otak rentan mengalami kerusakan pada kondisi kekurangan oksigen.

Jika sama sekali tidak mendapat suplai oksigen dalam waktu 3-7 menit saja, sel-sel otak akan mulai mengalami kematian.

Otak manusia memiliki berat rata-rata 1,4 kg (1.400 gram) dan ada sekitar 100 miliar neuron atau terdapat sekitar 70 juta neuron per gram. Sel-sel ini harus mendapatkan oksigen penuh agar kerjanya maksimal.

Manusia akan sekarat ketika tubuh tidak bisa mendapatkan asupan oksigen yang diperlukan untuk bisa bertahan hidup. Sehingga tidak heran bantuan oksigen adalah hal yang pertama diberikan jika seseorang pingsan agar jantung dan otaknya tetap mendapatkan oksigen.

Oksigen yang banyak artinya tubuh seseorang sehat. Makanan dan pola hidup yang sehat bisa meningkatkan jumlah oksigen di tubuh.

Begitu juga dengan olahraga pernapasan bisa meningkatkan kapasitas pengangkutan oksigen ke dalam darah. Oksigen yang cukup bisa meningkatkan proses metabolisme, karena tingkat oksigen yang berlebih ini akan meningkatkan kemampuan sel-sel untuk menggunakan lemak sebagai energi.

Latihan pernapasan menggunakan diafragma akan memungkinkan seseorang untuk menghirup napas lebih panjang dibandingkan dengan napas melalui dada, sehingga lebih banyak oksigen yang masuk ke dalam sistem.

Dengan melakukan latihan pernapasan yang rutin, maka seseorang bisa melatih tubuh untuk meningkatkan jumlah oksigen yang masuk ke dalam darah.

Di lain pihak oksigen dalam tubuh tidak bisa maksimal karena polusi udara, kurang tidur, menutup kepala saat tidur, merokok, zat-zat kimia, obat-obatan dan makanan tertentu.

Kekurangan oksigen bisa menimbulkan banyak penyakit seperti kerusakan batang otak (traumatic brain injury) dan down syndrome (keterbelakangan mental).

Anak yang ketika bayi mengalami kekurangan oksigen biasanya dalam masa pertumbuhannya akan mengalami kesulitan belajar, ketidakmampuan berkonsentrasi, masalah keseimbangan dan koordinasi tubuh. Autisme dan epilepsi juga diduga terkait dengan kekurangan oksigen saat lahir.

(ir/ver)


NB: utk atasi penyempitan pembuluh darah yg berakibat pengurangan pasokan oksigen ke otak, herbal yg direkomendasikan :
1. Daun dewa utk atasi pengentalan darah
2. pegagan utk elastisitas pembuluh darah
3. sambiloto utk atasi kolesterol yg menyumbat di pembuluh darah
 

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