I am beyond excited about two things today:
1. The 'Ancestral Weight Loss Registry'
2. The Human Food Project (The American Gut Project)
These two projects demonstrate that 'Ancestral' nutritional plans (and other generally low-carb plans), are NOT just "a crazy extremist fringe elitist caveman fairytale," that they are supported by GOOD scientific research, and that they are willing to stand the test of rigorous scrutiny (they've already stood the test of time).
In particular, the Ancestry is solidifying an easily accessible, well documented resource available to anyone with the courage to challenge what they think they know.
Check it out for yourself (you won't find a more transparent community... and by any standards this is a mind-boggling resource):
The image just above is a pictorial representation of the Ancestral Weight Loss Registry... the currently posted results are based on a sample of the first 1100 people to register from all 50 U.S. states and over 32 countries around the globe.
WHY? "There is much clinical and anecdotal evidence that a diet high in protein, fats, and vegetables may be an effective way to lose weight and improve health." AWLR
"The goal of the Ancestral Weight Loss Registry is to collect those anecdotes, standardize them, and quantify them so that instead of telling your friend or doctor about this one guy that did this caveman thing that helped him lose a bunch of weight, you can point to the AWLR as a collection of thousands of people succeeding (or not; it’ll all be included) with a paleo, Primal, or low-carb diet. In time, with enough registrants, the AWLR hopes to identify trends in health and nutrition. What works, what doesn’t, who succeeded, who didn't. People like to call paleo/Primal/ancestral a diet fad. A crazy extremist fringe elitist caveman fairytale. You know, there’s a small possibility they have a point, but if people sign up with the Ancestral Weight Loss Registry, we’ll be one step closer to knowing for sure."
"The AWLR has about 1200 registrants, as of now. That’s not bad for six and a half months, especially considering the National Weight Control Registry’s only done 6000 in 20 years." MARK SCISSON
SAFETY & EFFICACY OF CARB RESTRICTION
Safety and Efficacy of Diets Low in Carbohydrates
In clinical trials:
•A carbohydrate-restricted, calorie unlimited diet often results in more weight-loss than a calorie restricted, low-fat diet
•Carbohydrate-restricted diets decrease triglyceride levels
•Carbohydrate-restricted diets tend to increase HDL
•Diets high in protein tend to be more filling
The appearance and sudden popularity of the Atkins diet in the 1990s had dieters running to the meat department, leaving carbs in the dust. The apparent success of this diet, mostly ascertained from anecdotal evidence, had the overweight population excited and health experts worried. A diet characterized by high amounts of meat and fat was deemed impossible to be effective and a serious health risk.
At the time, few clinical trials had been done analyzing the efficacy and safety of such a diet, which understandably led to extreme scepticism among dieticians and doctors. Recent years have seen numerous such studies comparing a calorie unlimited, low carbohydrate diet to other popular diets, such as the ultra low-fat Ornish diet, or the calorie restricted generally accepted healthy diet promoted by the government, with a majority of calories coming from carbs. In other words, eat until you are full and limit carbs, or eat until you reach a calorie limit and restrict fat.
To the surprise of many, when compared to other diets, the calorie unrestricted, lowest carbohydrate diet group generally — but not always — loses more weight. With few exceptions, their HDL increases and their blood triglyceride levels decrease without having any significant effect on LDL (bad cholesterol). When subjects keep their carbohydrate intake lower than 50 grams per day, they seem to be most successful.
Often times the various groups fare the same, both losing approximately the same amount of weight. But never, in dietary clinical trial history, has a the low-fat, low-calorie diet resulted in more weight loss than a low-carb diet (If you can find one, please e-mail it to me and I will post it).
The High-Fat Paradox
The very idea that a diet characterized by high-fat foods and unlimited calories can do as well, or better, than a low-fat, calorie-restricted diet poses a challenge to the current weight-loss recommendations. Since fat has 9 calories per gram and protein or carbs have 4 calories per gram, a high fat diet seems destined to fail.
Two scenarios could potentially explain this paradoxical phenomenon, both of which seem to shed positive light on carbohydrate-restricted diets.It is possible that the simple act of eating high-protein, high-fat foods causes people to spontaneously eat less total calories. It has been tested and proven many times, that subjects who eat a high-protein meal report being more satisfied and often eat less in the following meal (see satiety). With this explanation, it seems that the regulation of calorie intake does not happen consciously, but rather at the cellular level, sending signals perceived consciously as fullness.
Another explanation, championed by many low-carb enthusiasts, is that carbohydrates, especially refined ones, cause weight gain via their stimulatory effects on insulin, the main hormone required for fat storage. Many foods spike insulin to varying degrees, but breads, pastas, sugars and refined flours are particularly potent. The USDA-promoted diet, consisting of 65% of one's daily calories deriving from carbohydrates, stimulates net insulin secretion to a greater degree than a low carbohydrate diet. As the theory goes, this excess insulin release may be chronically directing more calories into your fat cells as opposed to your body to be burnt for fuel. This, in turn, will cause the person to remain hungry since a certain amount of necessary energy did not reach the cells but rather was stored away as fat, perpetuating a vicious cycle of hunger co-existing with adipose tissue growth.
This hypothesis implies that calories are secondary in relation to how many carbs you eat. Many of the studies listed below which measured calorie intake seem to support this theory, since the subjects consuming the carbohydrate-restricted diet did not report eating less calories, and often lost more weight. However this is still unclear.
The mechanism by which this extra weight loss occurs remains controversial, but the positive effects of losing the weight is not. In general, the weight loss seems to be most dramatic during the first six months and sometimes levels off after a year or two. The subjects become less compliant to the diet as time goes on, making it impossible to tell if the diet doesn’t work after six months, or the subjects are just not following it properly.
Regardless of the mechanism, carbohydrate-restricted diets seem to be the most effective way to lose weight based on the clinical data. From a practical standpoint it seems logical that the majority of calories consumed on a successful diet should come from the most satiating nutrients. The clinical trials suggest that the simple act of placing someone on a carbohydrate-restricted diet is the only intervention and education required for the patients to lose weight. Their own internal hunger and satiety mechanisms regulate their food intake, making calorie counting unnecessary.
Critics of low carb diets point to the fact that protein spikes insulin as well as carbohydrates. Yet fat does not, so the hypothesis predicts that insulin would be elevated to a lesser degree in a diet made up mostly of non-starchy vegetables, meats and fats. Since meats consist of protein (which does spike insulin) and fat (which does not), and non-starchy vegetables have minimal insulin-effects, there is likely less total insulin release. If there is less net insulin circulating in your blood throughout a day or week or month, then one would expect less calories would be stored, and more calories would be released from your adipose tissue.
But perhaps the most common argument against a low-carbohydrate diet has been it’s potential long term negative effects on the heart. Since these diets are typically characterized by high amounts of saturated fats that raise total cholesterol (as well as HDL and LDL), they may be unhealthy when eaten for a long period of time. In the dietary clinical trials involving weight loss (as seen below), the cholesterol and LDL levels of the subjects eating the high saturated fat, low carb diets rarely increase much. However, the increased weight loss accompanying this diet may mask the effects that saturated fats have on blood cholesterol.
Since the 1960s there have been a relatively small number of clinical trials testing the dangers of a high saturated fat diet, usually in the absence of weight loss. Some were randomized, and some were not; some contained less than 100 subjects while others enlisted over 40,000; some show a large decrease in heart disease rates, and many do not. Despite 50 years of research, the results are inconclusive at best. The only two randomized, double blind studies ever done, lasting 4.5 years and 8 years respectively, found no decrease in heart disease. For a full list of all the clinical trials, and a more in depth analysis, see saturated fats and heart disease.
These results don’t necessarily imply that the such a diet is the magic bullet for everyone; or that anyone who follows one will suddenly become skinny and healthy. However, in clinical trials when a low-carb diet is compared to another diet, the subjects eating less carbs usually lose more weight and improve their HDL and triglyceride levels.
FOLLOW THE SCIENCE (studies detailed/linked at the AWLR)
DIETARY CHOLESTEROL & HEALTH EFFECTS
Dietary Cholesterol and Blood Cholesterol
•Dietary cholesterol has minimal effect on serum cholesterol compared to saturated fat
•Feeding studies provide mixed evidence, however meta-analyses point to a lack of major effect
•Those with very low baseline dietary cholesterol respond more than those with modest baseline cholesterol intake
•Adding 300-400 mg cholesterol to a cholesterol free diet results in an increase in serum cholesterol, but subsequent addition of more cholesterol has little, if any, effects
The idea that dietary cholesterol increases blood cholesterol seems very logical, however the evidence supporting this hypothesis suggests a very weak relationship. Dr. Ancel Keys was one of the first researchers to test this hypothesis, feeding subjects extremely high levels of dietary cholesterol and measuring their blood response. He found almost no effects, despite absurd amounts of dietary cholesterol. Upon further research, Keys accepted that there is some relationship, and created a formula to predict it: blood cholesterol is proportional to the square root of the amount of dietary cholesterol added.
Change in serum cholesterol between 2 diets = 1.5*(Z2 – Z1), where Z is the square root of the cholesterol content of each diet in mg/1000 kcal
According to Keys’ equation above, if someone consuming a 2,000 calorie diet and 1200mg of cholesterol (4x the recommended level) per day reduced their total dietary cholesterol by 6-fold to 200 mg a day, their serum cholesterol would drop by 21.75 mg/dl. Going from 300 mg per 1000 calories eaten to 150 mg per 1000 calories eaten would drop serum cholesterol by a mere 3.75 mg.
During the same time, other researchers believed there was a larger relationship. When they fed subjects cholesterol combined with egg yolk, their blood cholesterol increased. When they consumed much higher doses of pure cholesterol, the blood response was less pronounced. Possible explanations for this were increased bioavailability of the cholesterol when mixed with egg yolk, or the possibility that another ingredient besides the yolk’s cholesterol was increasing blood cholesterol levels. However, the amount of egg yolk required to make a significant difference is usually quite large.
Other researchers have since confirmed Ancel Keys’ square root relationship, adding that dietary cholesterol has greatest effects on serum cholesterol if it is added to a low cholesterol, or cholesterol-free diet. At moderate cholesterol intakes, serum cholesterol changed very little with added cholesterol. A 1997 meta-analysis compiled 9 predictive equations since 1990, calculating that for a 2500 kcal diet, a 1.37-2.68 mg/dl decrease in serum cholesterol could be expected for every 100 mg/day decrease in dietary cholesterol. The prediction based on their meta-analysis was a 2.2 mg/dl decrease in serum cholesterol for every 100 mg/day decrease in dietary cholesterol.
The American Heart Association recommends eating less than 300mg of cholesterol per day. This seems somewhat futile given the predictions above, and rather unattainable for the omnivore considering one 6 ounce piece of chicken breast has 168 mg. It also encourages low-protein diets, which seem to be less effective for weight loss and satiety. To decrease blood cholesterol, the research suggests that focus should be placed on replacing saturated fats with polyunsaturated fats, although the benefits to doing this seem futile. Limiting dietary cholesterol seems to have little benefit.
FOLLOW THE SCIENCE (studies detailed/linked at the AWLR)
• The Great Cholesterol Myth
SATURATED FATS AND HEART DISEASE
Saturated Fats and Heart Disease: The Clinical Trials
•Dietary saturated fats increase blood cholesterol levels in feeding studies
•Replacing saturated fats with polyunsaturated fats decrease cholesterol levels
•The only 2 double-blind, randomized trials in history failed to show that a low-saturated fat diet decreases heart disease
•3 meta-analyses published in the past 3 years concluded no decrease in heart disease associated with low saturated fat diet
In 1953, Ancel keys published the seminal 6-country ecologic study that found a striking correlation between total fat intake and cardiovascular mortality. It was based on his observations that increased meat consumption in America coincided with a rise in heart disease rates. This finding ignited the diet-heart hypothesis, linking dietary fat to cardiovascular disease.
Since the 1950s, there have been a relatively small number of large, long-term clinical trials examining the potential benefits of decreased saturated fats in the diet as a primary focus. All major trials since 1966 are listed in the bibliography below. Some took place in mental institutions, some were not randomized, and some also involved major confounding interventions such as weight loss, exercise, or increased fruit and vegetable consumption. Some show benefits to replacing saturated fats with polyunsaturated fats, while others do not.
If we were to focus on the largest (i.e. > 100 subjects), randomized, most famous trials ever done lasting longer than 1 year, we are left with very few to assess that meet the following 2 criteria:
1) The only significant intervention involved a reduction in fat and saturated fat and an increase in polyunsaturated fats
2) They ask the question: does this diet reduce heart disease? (defined as heart attacks or death from heart disease)
Listed in reverse chronological order:
Women’s Health initiative (2006) – 48,835 women, 8 years, no significant difference between intervention and control.
Diet and Reinfarction trial (1989) – 2,033 men, 2 years, no significant difference between the groups given and not given fat and fiber advice. No significant differences in ischaemic heart disease between intervention and control (intervention was only advice in this trial)
Minnesota Coronary Survey* (1989) – 4,393 men and 4,664 women, double-blind, 4 years, no significant reduction in cardiovascular events or total deaths from the treatment diet
Finnish Mental Hospital (1972) – 12 years, physicians not blinded, significant decrease in coronary heart disease (CHD)death in men ( 5.7 deaths /1000 person-years vs 13 deaths /1000 person-years in the control. Non-significant decrease in CHD in women. (Not randomized, although included here because this is main experiment cited in support of diet-heart hypothesis)
Los Angeles Veteran’s Trial* (1969) – 846 subjects, up to 8 years, non significant difference in primary endpoints – sudden cardiac death or myocardial infarction. More non-cardiac deaths in experimental group, resulting in near identical rates of total mortality
Oslo Heart Study (1968) – 412 men, 5 year, slight decrease in CHD with intervention. Many dietary interventions accompanied the low saturated fat diet. When stratified by age, the results were significant only in subjects younger than 60.
* Double blind
FOLLOW THE SCIENCE (studies detailed/linked at the AWLR)
OBSERVATIONAL HEART DISEASE STUDIES
Saturated Fats and Heart Disease: Observational Studies
•The majority of prospective cohort studies found no correlation between saturated fat intake and heart disease
•Poor dietary assessment methods and large potential for bias create strong limitations to this data
•Focus should be placed on improving dietary patterns and not incriminating one specific nutrient
Since the 1950s, saturated fat has been incriminated as the major dietary contributor to heart disease, attributed mainly to the fact that saturated fats have the ability to raise blood cholesterol. This temporary physiologic response to dietary fats led to the logical hypothesis that replacing saturated fats with polyunsaturated fats, which lower blood cholesterol, may also lower coronary heart disease (CHD) rates, cardiovascular mortality, or both. This biological response to saturated fats has been the main reason diets high in meats carry such a stigma. The best way to determine if this hypothesis is true is through randomized, clinical trials. As discussed on our Saturated Fats & Heart disease – Clinical trials page, the evidence from the past 60 years has been inconclusive.
Yet conducting a large, long term trial is tremendously expensive and burdensome. For these reasons, prospective cohort studies offer an alternative design, although no causation can be determined. Subjects can be followed for a very long time and associations between their diets and disease can be illuminated. However, these observational studies (also known as prospective cohorts) have many short comings as well.
When researchers study the possible negative effects of saturated fats in prospective cohorts, they perform a baseline dietary intake measurement (usually a Food Frequency Questionnaire (FFQ), 24-hour recall, or 7 day food record), then follow subjects for up to ~25 years. The majority of them do not assess the diet anywhere in between. Just day one (or week one), and year 25.
In other words, What did you eat today, then in 25 years I will check to see if you died of heart disease. If you did, then I will correlate that with your diet the day I asked you what you ate.
Of course the likelihood that the baseline assessment is representative of their diet for the next 25 years is low. The best baseline assessments were 7-day food records, where subjects meticulously weigh and record everything they ate. These were rare.
To complicate matters further, a large percentage of these cohorts used an FFQ to assess the baseline intake. Dr. Walter Willet, from the Harvard School of Public Health has demonstrated that FFQs can be quite inaccurate. In one validation study, the foods most accurately reported were tea and beer, while things like meat, fish, bacon, and hamburgers were at best 25% accurate. The subjects filling them out also had a tendency to under-report foods deemed unhealthy while over reporting fruits and vegetables. From the screen shot below of an actual FFQ used in a Harvard study asking adults to answer these questions about their diet as teenagers, it becomes apparent why it can be so inaccurate and subject to bias.
Never the less, researchers’ attempts to to find a link between saturated fats and heart disease have been unsuccessful for the most part. Some studies have found a correlation, usually of borderline significance, while many have not.
Trying to isolate saturated fats in the sea of nutrients, vitamins, and calories a subject’s diet consists of is difficult if not impossible, and leads to many correlations that may be misleading. For these reasons, it is likely more beneficial to focus on making more practical and tangible changes to the diet, such as eliminating processed foods and sugar or increasing your daily servings of fruits and vegetables.
FOLLOW THE SCIENCE (studies detailed/linked at the AWLR)
"We must admit that our opponents in this argument have a marked advantage over us. They need only a few words to set forth a half-truth; whereas, in order to show that it is a half-truth, we have to resort to long and arid dissertations." FREDERIC BASIAT
ANCESTRAL Weight Loss Registry Blog
• Dr. Mary Vernon on why carb-restriction works
• Men Vs. Women: Biggest challenges to adopting a paleo or carb-restricted diet
• Dr. Lustig explaining the carbohydrate-insulin-obesity relationship
• Amazing TED talk on Paleo diets as potential treatment for Multiple Sclerosis
Speaking of 'following the science', another important project to which SPARKlers could greatly contribute is 'The American Gut Project' via the 'Human Food Project':
Consider signing up! At least sign up for the newsletter and be part of the beginning sof a revolution in health and medicine!
"Although we know that the composition of our microbiome is important to our health, we’re still trying to figure out the many ways it affects (or, it could be said, creates) our health. We know a few things. In other words, we’re more bacteria than human. We can determine whether someone is lean or obese by looking at their gut flora. We know how the gut microbiome forms the first line of our immune system’s defenses, how it determines our sensitivities to foods, and how it is sensitive to all sorts of stressors. We also know that the microbiome has “something” to do with a range of health issues, like autism, IBS, cancer, diabetes, heart disease, autoimmune diseases… but it’s still very vague. And with our gut flora actually outnumbering our “native” human cells nine to one, we don’t know nearly enough about a crucial, incredibly vast aspect of ourselves that affects every facet of our health. In other words, we’re more bacteria than human, so we had better figure out what’s going on in there.
Jeff Leach of the Human Food Project thinks the key to health today is figuring out the composition of the ideal microbiome. Right now, there’s no solid, reliable reference point for a “perfect microbiome,” though. It simply doesn’t exist. What does the microbiome of an autistic patient look like? What about someone with irritable bowel syndrome? Colon cancer? How does a hunter-gatherer’s gut flora compare to a SAD dieter’s? What about a Primal Blueprint eater’s gut compared to a vegan’s gut? What we eat and how we live affect the composition of our microbiome, which in turn affects our susceptibility to various diseases, but how? How do you get from a “bad” microbiome to a “good” one? These are essential questions that we cannot answer conclusively. Not yet. But if you sign up for The Human Food Project, the world’s biggest crowdsourcing microbiome project in history, we might just get some answers." MARK SCISSON
(quote by CHRISTINE MASON MILLER)
...Because it's about the JOURNEY, not the destination!
JUST DO IT.
'BEFORE' Pictures (May 31, 2009 - September, 2011) & Continuing PROGRESS (February 2012)! Next pictures September 1, 2012!
(I'm now keeping these right under my nose... in addition to being part of every blog I post, they are printed off and taped to my bedroom mirror)
Measurements, Musings & Motivation to MOVE!
(UPDATED/rewritten: JUNE, 2012)
I've Reached My Goal Weight!!!!!!!
NOTE: My weight tracker is NOT a truthful representation of my weight. Instead, I am using it as a tool to help me visualize my goal as though it's already been achieved!
UNTIL. (My 'Just Do It' blog)
DONE Girl Love...
(the footsteps into which I place my own feet)
Why I'm STILL here... my SparkJourney Saga
Words CAN Be Enough... page 3
Paleo... Do you really know what you're talking about?