Matt Lentzner, Janine Jagger and I have designed a survey for participants of Gluten-free January, using the online application StatCrunch. Janine is an epidemiologist who studies healthcare worker safety at the University of Virginia; she has experience designing surveys for data collection so we're glad to have her on board. The survey will allow us to systematically gather and analyze data on the results of Gluten-free January. It will be 100 percent anonymous-- none of your answers will be connected to your identity in any way.
This survey has the potential to be really informative, but it will only work if you respond! The more people who take the survey, the more informative it will be, even if you didn't avoid gluten for a single day. If not very many people respond, it will be highly susceptible to "selection bias", where perhaps the only people who responded are people who improved the most, skewing the results.
Matt will be sending the survey out to everyone on his mailing list. Please complete it, even if you didn't end up avoiding gluten at all! There's no shame in it. The survey has responses built in for people who didn't avoid gluten. Your survey will still be useful!
We have potential data from over 500 people. After we crunch the numbers, I'll share them on the blog.
Senin, 31 Januari 2011
Kamis, 27 Januari 2011
The Diabetes Epidemic
The CDC just released its latest estimate of diabetes prevalence in the US (1):
These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.
The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.
Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.
* In other words, it's the best predictor of future diabetes risk.
** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).
Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):
These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.
The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.
Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.
* In other words, it's the best predictor of future diabetes risk.
** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).
Two Wheat Challenge Ideas from Commenters
Some people have remarked that the blinded challenge method I posted is cumbersome.
Reader "Me" suggested:
Reader "Me" suggested:
You can buy wheat gluten in a grocery store. Why not simply have your friend add some wheat gluten to your normal protein shake.Reader David suggested:
They sell empty gelatin capsules with carob content to opacify them. Why not fill a few capsules with whole wheat flour, and then a whole bunch with rice starch or other placebo. For two weeks take a set of, say, three capsules every day, with the set of wheat capsules in line to be taken on a random day selected by your friend. This would further reduce the chances that you would see through the blind, and it prevent the risk of not being able to choke the "smoothie" down. It would also keep it to wheat and nothing but wheat (except for the placebo starch).The reason I chose the method in the last post is that it directly tests wheat in a form that a person would be likely to eat: bread. The limitation of the gluten shake method is that it would miss a sensitivity to components in wheat other than gluten. The limitation of the pill method is that raw flour is difficult to digest, so it would be difficult to extrapolate a sensitivity to cooked flour foods. You might be able to get around that by filling the pills with powdered bread crumbs. Those are two alternative ideas to consider if the one I posted seems too involved.
Senin, 24 Januari 2011
Blinded Wheat Challenge
Self-experimentation can be an effective way to improve one's health*. One of the problems with diet self-experimentation is that it's difficult to know which changes are the direct result of eating a food, and which are the result of preconceived ideas about a food. For example, are you more likely to notice the fact that you're grumpy after drinking milk if you think milk makes people grumpy? Maybe you're grumpy every other day regardless of diet? Placebo effects and conscious/unconscious bias can lead us to erroneous conclusions.
The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.
Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.
Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?
Procedure for a Blinded Wheat Challenge
1. Find a friend who can help you.
2. Buy a loaf of wheat bread and a loaf of gluten-free bread.
3. Have your friend choose one of the loaves without telling you which he/she chose.
4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.
5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.
6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.
7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.
If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.
* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.
** More subjective forms of inquiry have their own advantages.
The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.
Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.
Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?
Procedure for a Blinded Wheat Challenge
1. Find a friend who can help you.
2. Buy a loaf of wheat bread and a loaf of gluten-free bread.
3. Have your friend choose one of the loaves without telling you which he/she chose.
4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.
5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.
6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.
7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.
If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.
* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.
** More subjective forms of inquiry have their own advantages.
Twist Series: Growth & Length Retention IV
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| Micro twists (real hair) |
- I want to know how often should you moisturize in twists? I tend to do it everyday, and my hair ends up fuzzy!
I moisturize 1x a week, thus minimizing frizz, fuzz, and shrinkage. I'm a big believer that if a moisturizer is doing what it's supposed to do, one wouldn't have to use it daily. Try experimenting with other products if the one you are using just isn't keeping your hair moisturized. Additionally, look into what you are using for your deep conditioner. In my experience, a good deep condition and moisturizer on the day of twisting is key! (Other than this method, you can plait your twists until they airdry to minimize the fuzz.)
- at what length should you start wearing twists for length retention? i have about eight inches of hair all around and any time i try to do twists, it just looks ridiculous if i don't pin it up into a style. should i just refrain from doing twists until i get more length?
You can start wearing twists at any length that you are able to do so. I will admit that when my hair was shorter, I felt ridiculous wearing twists to work. However, after playing with them for some time, I was able to find a "suitable" style that was comfortable for me. Eight inches is actually a good length for versatile twist styles. In the next post, I'll include some pictures of style ideas for all lengths. Stay tuned ...
_____________________
In case anyone has missed previous Q&As, check out this Twist Series recap. Feel free to post any more questions in the comment section below:
Twist Series: Growth & Length Retention III
Twist Series: Growth & Length Retention II
Twist Series: Growth & Length Retention I
Twist Series: Washing & Matting
Twist Series: How to Flat Twist
Twists Series: Method II
Twist Series: Frizz and Knots
Twist Series: The Method I
Twists Series: Maintenance II
Twist Series: Maintenance I
Jumat, 21 Januari 2011
3in6 Challenge Rules
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To all the challengers (and interested readers), be sure to bookmark this post!
Purpose of this challenge: To retain 2-3 inches of growth in 6 months.
Challenge period: February 1 - August 1, 2011
Guidelines:
1. Eat fresh vegetables or fruits with each meal.
2. Take a daily multivitamin.
3. Drink sufficient water.
(Amt of water in oz. = Your weight in lbs * 0.5)
4. Wear twists or braids 2-4 weeks at a time.
5. No direct heat.
6. Pre-poo with coconut oil for 20 minutes.
7. Absolutely no trimming. (Start with a fresh cut now if need be.)
Allowances:
Each challenger is allowed two 1-week periods of styling her hair as she pleases (e.g., puff, rollerset, etc.).
For documentation of your length retention:
- Notebook/journal or camera
- Ruler/measuring tape
Tips on wearing twists/braids long term:
- Do not twist/braid too tightly
- Redo the perimeter weekly or biweekly.
- Deep condition & detangle thoroughly prior to twisting or braiding.
- For more tips, check out posts in the twist series
The Challenge begins February 1st! Start preparing.
Kamis, 20 Januari 2011
Eating Wheat Gluten Causes Symptoms in Some People Who Don't Have Celiac Disease
Irritable bowel syndrome (IBS) is a condition characterized by the frequent occurrence of abdominal pain, diarrhea, constipation, bloating and/or gas. If that sounds like an extremely broad description, that's because it is. The word "syndrome" is medicalese for "we don't know what causes it." IBS seems to be a catch-all for various persistent digestive problems that aren't defined as separate disorders, and it has a very high prevalence: as high as 14 percent of people in the US, although the estimates depend on what diagnostic criteria are used (1). It can be brought on or exacerbated by several different types of stressors, including emotional stress and infection.
Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.
During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.
Here's what I take away from this study:
I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?
* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.
** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.
*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.
Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.
During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.
Here's what I take away from this study:
- Wheat gluten can cause symptoms in susceptible people who do not have celiac disease.
- A lack of circulating antibodies against gluten does not necessarily indicate a lack of gluten sensitivity.
- People with mysterious digestive problems may want to try avoiding gluten for a while to see if it improves their symptoms**.
- People with mysterious fatigue may want to try avoiding gluten.
I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?
* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.
** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.
*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.
Rabu, 19 Januari 2011
Twist Series: Growth & Length Retention III
- how can you protect your ends while in twists?
- ... What products should you use?
- ... and should end papers be used to protect ends?
- ... Also how long should you keep twists in for optimal growth? Should you keep a style in one, two or three weeks
Label of the Day: Breakage
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| {Image Source} |
Tips for a Sensitive Hairline
Tips for Transitioning or Stretching Relaxers
Nape Breakage?
Micro Twist Takedown on CNapp Hair
Boar Brush = Damage to Your Edges?
For more breakage-related posts, click here.
Selasa, 18 Januari 2011
3 inches in 6 months Challenge!
Hair grows an average of 0.5in/month. (Some people get less growth and others get more.) For this challenge, we'll aim to retain 2-3 inches in 6 months. Guidelines will be posted later this week to help you through the process. Also, we'll be in touch on a monthly basis. If you are interested, please leave a comment below.
Challenge period: February 1 - August 1, 2011.
Healthy hair in 2011!
Minggu, 16 Januari 2011
Decolonization and Animal Liberation: Love, Violence, Becoming-Other-Wise
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| Beehive Design Collective. "FTAA." Source: www.beehivecollective.org |
Some cyber-friends have been pestering me to put up another blog post since I haven't posted anything in three months--well, maybe that's an exaggeration but i really wanted to use the word pestering--, so I'm posting two abstracts I recently submitted to the Thinking About Animals conference at Brock University (St. Catharines, ON, Canada) going on between March 1 and April 1, 2011. This will be the 10th Critical Animal Studies conference, and Brock is perhaps one of the most deserving universities since its establishment of a critical animal studies minor and an official vegan policy in the Sociology department.
On that note, I encourage you to check out the Critical Animal Studies resource page I created over winter break!!!
The first paper, on Frantz Fanon's The Wretched of the Earth, is a paper I wrote for Existentialism in the Fall. I went through some angst writing it, but came out overall satisfied with the paper. If any of you are interested in reading it, I'll send you a copy in exchange for some good feedback. The second paper ought to be more familiar to avid readers of this blog. It's basically a summation of what I have written on the understanding of veganism over the last two years or more.
1.
Decolonization and Animal Liberation:
Violence and Becoming-Animal in Frantz Fanon’s The Wretched of the Earth
In 1961, the Algerian psychoanalysist, Frantz Fanon, published, Les Damnés de la Terre, a book specifically about the revolutionary movement in French Algeria, but a guide to decolonization in general. In The Wretched of the Earth, Fanon gives a phenomenological account of the Algerian independence movement, from its inception in local, spontaneous violent uprisings, to a national political movement, to the development of a national culture and new humanism. For Fanon and his friend Sartre, violence is a necessity for the colonized to become fully human and political subjects. Similarly, the development of a national culture is necessary development for not only the liberation of Algeria, but for the future of humanity.
While Fanon’s primary goals are the achievement of national consciousness and a new humanism, a subversive reading of this text foregrounds “the animal” that beseeches his description of decolonization. Fanon’s characterization of the relationship between decolonization and animals is complex: on the one hand, animal being is to be transcended, if not negated through self-assertion and violence, yet the animal virtues of spontaneity, ferocity, and pack-forming are crucial for the overthrow of the colonizers. If humans’ metaphoric relationship to “animality” and animal others materialize in their relationship with one another, as is argued, then decolonization will not be achieved so long as a hierarchical and exclusionary identity politics exists between human and animal others (as is inferred by Fanon and Sartre’s subject-centered humanist discourse). It is argued that the anarchistic process of “becoming-animal” described by Gilles Deleuze and Félix Guatarri is a more transformative and promising alternative to humanism for not only human liberation, but also the liberation from humanist violence against “animality” and animal others.
2.
Deconstructing Veganism:
Love, Listening, Conversations, and Companionships Beyond Boundaries
For over a decade, Gary Francione (1996, 2008) has been championed for his bold challenge to the efficacy of “new welfarism” and the sufficiency of lacto-ovo-vegetarian advocacy in the contemporary “animal rights” movements. Yet relatively few animal abolitionists have ever challenged the sufficiency and status quo of veganism. In a time when neoliberalism has come into a greater appropriation of veganism (Hammer 2008), real animals have become absent from the discourse of many animal and vegan advocacy campaigns (Adams 2006), and to be a vegan is more about one’s way of life (i.e. the subculture one belongs to) than one’s actual relationship to animals, a more radical critique of not only vegetarianism but veganism too is needed.
While many celebrate the mainstreaming of veganism, I would like to caution self-identified vegans and animal activists from accepting the present understanding of vegan as an identity of (abstention from) consumption. The present understanding of veganism as a) an identity b) defined negatively as an abstention from c) consumption has lead to a certain modality of political and private life which has been legitimately accused of self-righteousness, identity politics, militancy, colonialism, and privileged consumerism. In light of this, we are called to a radical rethinking of veganism not as a noun (“ vegan”) to be identified with, purchased, consumed, and completed, but as a modality and relationship with others that is never yet complete.
Veganism is something to be understood affirmatively, as an affirmation of our own feelings and the voices of others. Those who have come into veganism as a liberation project must adamantly recall that they did not do so because of convenience, out of tradition, or merely out of pleasure, but because they are in search of affirming love. This love must never be forgotten as their point of departure and arrival. The ends of veganism are in the means of not forgetting, disavowing others. It is through disavowal that people commit the most violence by ignoring their own and others’ sentiments; they wage war on themselves and others for foreclosing ends, ideals, and identities, rather than waging conversation. The end of veganism is thus not to become a vegan, but to become other-wise in conversations and companionships beyond boundaries and “language.”
Read more »
Jumat, 14 Januari 2011
Youtube: HEALTHY Food Recipe for the Professional
Check out the following informative video from one my favorite youtubers. I've been making my own ground turkey tacos for some time and love to see when others are taking the healthier route as well. She (Afrostory) does a thorough job of explaining alternatives to ground beef, cheese, salsa, and iceberg lettuce. She also gives insight into the effects of high sodium, processed salt, lactose intolerance, etc.
If you're on a budget, check out the following DIY healthy smoothie recipes in place of Odwalla:
Soy Smoothie Meets Green Smoothie
Cranberry Smoothie
Again, healthy hair and body start from within!
If you're on a budget, check out the following DIY healthy smoothie recipes in place of Odwalla:
Soy Smoothie Meets Green Smoothie
Cranberry Smoothie
Again, healthy hair and body start from within!
Chapt.II: Precautions When Highlighting
This week, I'll discuss some precautions one should take when highlighting natural hair at home. If you choose to have the process done professionally, be sure that your colorist knows how to color natural hair and not just hair in general. I had a friend walk into an Aveda salon and walk out with beautiful color but loosened texture and dry hair. Don't let that be you.
PRECAUTIONS when highlighting at home:
1. Use a commercial kit. Commercial highlighting kits are designed to yield minimal mistakes. I have used (in the past) and recommend African Pride HiLites. L'Oreal Colour Rays (used this time) is also good but TOO strong for relaxed tresses. Though a few people have had success with hydrogen perioxide as a highlighting technique, I do NOT recommend it (from my own past experience); by the time it lifts the color to a desirable shade, damage is done to the strands.
2. FOLLOW THE DIRECTIONS provided in the kit. This is the number one precaution one must take above all others. Many highlight jobs go wrong when instructions are not followed properly. I've had the experience of my whole hair break off when I left a dye on for 5 minutes longer than stated in the directions.
3. Pre-treat with coconut oil for 20 minutes before highlighting. I don't know whether this method is effective against chemical damage or merely psychological, but I felt better knowing that my hair was strengthened going into the dye job. The oil did not interfere with the intensity of the color in my experience.
4. Don't leave the dye on your head longer than instructed. Actually, it is ideal to leave it on for less time. If the kit says 25 minutes, leave it on for 20 minutes. If you want optimal color, leave it on for the full 25 minutes but no longer than that.
5. Rinse and wash your hair and scalp thoroughly after the process.
6. After using the conditioner/conditioning shampoo from the kit, follow up with your usual deep conditioner. This step will ensure that moisture and strength is restored to your strands. In my recent highlighting experience, I immediately followed up with a 20-minute deep treatment using Lekair Cholesterol mixed with olive oil.
7. Wait about 4-6 months to highlight after a henna treatment. (See this link.) After highlighting, wait another 4-6 months before hennaing again. Some individuals may highlight/henna sooner, but this precaution is just to be on the safe side.
NEXT WEEK ... MAINTENANCE TIPS
Kamis, 13 Januari 2011
Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational Studies
The diet-heart hypothesis states three things:
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These studies show that saturated fat increases both LDL cholesterol ("bad cholesterol") and HDL cholesterol ("good cholesterol"), but typically the former more than the latter. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between habitual saturated fat intake and blood cholesterol, it has been very small or nonexistent. Those findings are rarely cited, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments. [UPDATE 4-2012: I did miss several studies, although they're basically consistent with the conclusion I came to here. I plan to update this post with the new references at some point.]
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method is much more accurate than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They analyzed the data every which way, but were never able to squeeze even a hint of an association out of it:
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends very little support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was roughly 3/4 white rice by calories. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and had a very peculiar and perhaps deficient diet. Also, what is the difference between a diet with 5 and 75 grams of saturated fat per day? Those diets are probably very different, in many other ways than their saturated fat content.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold difference in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's much less influential than other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat a diet that differs in many ways from the diets at the upper end of the range, and other aspects of lifestyle such as physical activity also differ.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol in humans. If it's a factor at all, it must be rather weak. It may be that the diet-heart hypothesis rests in part on an over-reliance on the results of short-term controlled feeding studies. It would be nice to see this discussed more often (or at all) in the scientific literature. It is worth pointing out that the method used to collect diet information in most of these studies, the food frequency questionnaire, is not particularly accurate, so it's possible that there is a lot of variability inherent to the measurement that is partially masking an association. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a modest long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators did not attempt to adjust for confounding factors.
- Dietary saturated fat increases blood cholesterol
- Elevated blood cholesterol increases the risk of having a heart attack
- Therefore, dietary saturated fat increases the risk of having a heart attack
The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.
Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These studies show that saturated fat increases both LDL cholesterol ("bad cholesterol") and HDL cholesterol ("good cholesterol"), but typically the former more than the latter. These are the studies on which the diet-heart hypothesis was built.
But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?
I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between habitual saturated fat intake and blood cholesterol, it has been very small or nonexistent. Those findings are rarely cited, but let's have a look...
The Studies
It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments. [UPDATE 4-2012: I did miss several studies, although they're basically consistent with the conclusion I came to here. I plan to update this post with the new references at some point.]
The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method is much more accurate than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They analyzed the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk***.
The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends very little support to the hypothesis.
Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).
This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was roughly 3/4 white rice by calories. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and had a very peculiar and perhaps deficient diet. Also, what is the difference between a diet with 5 and 75 grams of saturated fat per day? Those diets are probably very different, in many other ways than their saturated fat content.
In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold difference in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's much less influential than other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat a diet that differs in many ways from the diets at the upper end of the range, and other aspects of lifestyle such as physical activity also differ.
The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no relationship between saturated fat intake and blood cholesterol.
Conclusion
Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.
Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol in humans. If it's a factor at all, it must be rather weak. It may be that the diet-heart hypothesis rests in part on an over-reliance on the results of short-term controlled feeding studies. It would be nice to see this discussed more often (or at all) in the scientific literature. It is worth pointing out that the method used to collect diet information in most of these studies, the food frequency questionnaire, is not particularly accurate, so it's possible that there is a lot of variability inherent to the measurement that is partially masking an association. In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a modest long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.
The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL
* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.
** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.
*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.
**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators did not attempt to adjust for confounding factors.
Selasa, 11 Januari 2011
Dr. Fat
A blog reader recently made me a Wordle from Whole Health Source. A Wordle is a graphical representation of a text, where the size of each word represents how often it appears. Click on the image for a larger version.
Apparently, the two most common words on this blog are "Dr" and "fat." It occurred to me that Dr. Fat would be a great nom de plume.
Apparently, the two most common words on this blog are "Dr" and "fat." It occurred to me that Dr. Fat would be a great nom de plume.
Chocolate Conditioner Recipes!
CHOCOLATE HAIR MASK
- dark chocolate bar
- yogurt
- honey
Recipe and Instructions
CHOCOLATE & BANANA HAIR MASK
- overripe banana (be sure to sieve)
- honey
- dark chocolate
Recipe and Instructions
CHOCOLATE HAIR MASK - For the Mixologist!
- honey
- overripe banana
- coconut milk
- coconut oil
- pure cocoa butter
- jojoba oil (or olive oil)
- pure cacao (cocoa) powder
Recipe and Instructions
1. CAFFEINE AND BALDING
Twist Series: Growth & Length Retention II
- While maintaining twists, how can you prevent the ends from getting tangly (scraggly)?
- i second the question on how to prevent tangly ends while in twists. they feel detangled before i twist them, but when i take them down i sometimes feel the tangles.
- How often should you trim while wearing twists?
- When is the best time to start pinning them up? I'm noticing that I'm losing some length due to damage at the ends, though I've been wearing my hair in twists as a protective style for the past few months.
Jumat, 07 Januari 2011
Healthy Skin Tips for 2011
 |
| {Image Source} |
1a. Eat healthily
The number one key to healthy skin is to eat healthy. Great food choices include carrots (high in Vitamin A), green vegetables, oranges, etc. If you are not getting sufficient nutrients from your meals, invest in a good multivitamin. An antioxidant supplement couldn't hurt either. (For more info: antioxidants and aging.)
1b. Eat less sweets
Research has shown that sweets (eg., chocolate, candy, cake, etc.) may contribute to acne. From my own personal experience, I have seen this to be true with my skin. For the new year, replace sweets with granola bars, peanut butter on wheat sandwiches, and fruits. (For more info: sugar and acne, article on sugar and acne.)
2. Drink sufficient water
Water helps to move nutrients throughout the body.
3a. Adhere to a skin care regimen
A skin care regimen is also essential for achieving healthy skin. Wash daily and nightly. Exfoliate regularly. Invest in a good cleanser, moisturizer, and sunscreen. (For more info: basic skin care regimen.)
3b. Wear sunscreen
Even though "black don't crack", it eventually will and will do so at a faster pace without UV protection. Wear sunscreen containing a minimum SPF of 15. (For more info: black skin and sunscreen.)
Label of the Day: Moisture
1. Winterize Your Washes!
2. Winterize Your Conditioner!
3. Retaining The Hair You Grow: Chapter 6
4. Reader's Question: More on Moisture ... Dry Ends
5. Oils, Aloe Vera, and Whipped Butter
6. Whipped Hair Butter Recipes Galore!
7. Retaining the Hair You Grow: Chapter 7
8. Grapeseed Oil, Linoleic Acid, & Body Butter Mix
9. Reader's Question: When Shea Butter Doesn't Work
10. Moisturizing Spritz Recipes
Rabu, 05 Januari 2011
Chemically Highlight Natural Hair?
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| {Jordin Sparks} |
WHAT ARE THE RISKS?
Read this previous post on the chemical process and potential damage from misuse. Do your own research as well.
WHY CHEMICAL HIGHLIGHTS?
Why do you want chemical highlights? Can the color you are seeking be achieved by healthier, more natural means (e.g., henna, honey, cinnamon)? What about temporary alternatives (e.g., color extensions)?
IS YOUR HAIR HEALTHY?
If your hair is damaged and weak, I recommend staying away from chemical highlights. If your hair is healthy, are you willing to suffer any setbacks or consequences that may come with highlighting? Split ends? Increased porosity?
DO YOU HENNA?
Do you plan to henna after highlighting? Have you hennaed and now plan to chemically highlight? If so, there are some factors (e.g., length of time between dye job and henna treatment, quality of henna used, etc.) you should consider. Read this link and do further research.
Stay tuned for a post on PRECAUTIONS, MAINTENANCE, ETC.
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| {Highlights achieved with a semi-permanent commercial dye.} |
Twist Series: Growth & Length Retention I
- thanks for being so charitable as to provide this info for us thirsty readers! here's my query: since taking down my 10 year old locs, i have "dusted" my ends but not gone for a professional trim. i've worn my hair in some form of natural for 15 years now, but this is my first time really on a "length" journey, so i'm trying to familiarize myself with all the new products, info, and various strategies. As such, I am wondering how crucial regular trimming has been for you.
Regular trimming is very crucial for length retention because it removes damaged ends (e.g, split ends, single-strand knots, etc.). However, how you trim can determine whether you are actually retaining length or cutting away progress. I only trim my ends when needed as opposed to following a set schedule. For more details, on trimming for length retention, here is a repost:
--------------------
Freeze! Drop the scissors! Put your hands up! Stop cutting!
Excessive trimming can hinder length retention. If your hair grows six inches a year and you trim half an inch every month, then you are essentially cutting off all your growth progress. In order to retain length, you have to (1) be healthy from the inside out, (2) treat your hair right, and (3) pick up the scissors only when necessary. There is a time to trim that is not dictated by the calendar on the wall but by the health of the ends of your hair.
 |
| {May 2009} |
HEALTHY VS DAMAGED ENDS:
Healthy ends are free from splits and other damage. Splits are an indicator of damage to the cuticle and come in all shapes and sizes. Some occur at the very ends of the hair while others form in the middle of a strand. The hair may be appear to be split into two pieces or more. It is a myth that split ends can be repaired; some products may temporarily make them less visible, but splits cannot "heal" themselves and will exist until cut off. If you are taking great care of your hair, you will see fewer splits. Fewer splits = healthier hair. Healthier hair = fewer trims.
CUTTING DAMAGED ENDS:
Even if you've determined that your ends are damaged, a full-on trim may not be required. Search and destroy is a method for only cutting the strands that have splits or other visible damage. Dusting is a method of trimming a very small fraction of hair -- about 1/4 of an inch or less. Search and destroy and dusting are ideal for hair that exhibits a small amount of damaged ends. A full-on trim is needed when a large portion of the hair's ends are damaged.
MORE READS:
MINIMIZING SPLIT ENDS (great article btw)
SEARCH & DESTROY AND DUSTING
Senin, 03 Januari 2011
Paleolithic Diet Clinical Trials, Part V
Dr. Staffan Lindeberg's group has published a new paleolithic diet paper in the journal Nutrition and Metabolism, titled "A Paleolithic Diet is More Satiating per Calorie than a Mediterranean-like Diet in Individuals with Ischemic Heart Disease" (1).
The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).
One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).
With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.
There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.
A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).
A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.
If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.
*Intakes were determined using 4-day weighed food records.
**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.
The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).
One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).
With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.
There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.
A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).
A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.
If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.
*Intakes were determined using 4-day weighed food records.
**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.
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