This book was sent to me by Matt Schoeneberger, who co-authored it with Jeff Thiboutot. Both have master's degrees in exercise science and health promotion. S.P.E.E.D. stands for Sleep, Psychology, Exercise, Environment and Diet. The authors have attempted to create a concise, comprehensive weight loss strategy based on what they feel is the most compelling scientific evidence available. It's subtitled "The Only Weight Loss Book Worth Reading". Despite the subtitle that's impossible to live up to, it was an interesting and well-researched book. It was a very fast read at 205 large-print pages including 32 pages of appendices and index.
I really appreciate the abundant in-text references the authors provided. I have a hard time taking a health and nutrition book seriously that doesn't provide any basis to evaluate its statements. There are already way too many people flapping their lips out there, without providing any outside support for their statements, for me to tolerate that sort of thing. Even well-referenced books can be a pain if the references aren't in the text itself. Schoeneberger and Thiboutot provided appropriate, accessible references for nearly every major statement in the book.
Chapter one, "What is a Healthy Weight", discusses the evidence for an association between body weight and health. They note that both underweight and obesity are associated with poor health outcomes, whereas moderate overweight isn't. While I agree, I continue to maintain that being fairly lean and appropriately muscled (which doesn't necessarily mean muscular) is probably optimal. The reason that people with a body mass index (BMI) considered to be "ideal" aren't healthier on average than people who are moderately overweight may have to do with the fact that many people with an "ideal" BMI are skinny-fat, i.e. have low muscle mass and too much abdominal fat.
Chapter 2, "Sleep", discusses the importance of sleep in weight regulation and overall health. They reference some good studies and I think they make a compelling case that it's important. Chapter 3, "Psychology", details psychological strategies to motivate and plan for effective weight loss.
Chapter 4, "Exercise", provides an exercise plan for weight loss. The main message: do it! I think they give a fair overview of the different categories of exercise and their relative merits, including high-intensity intermittent training (HIIT). However, the exercise regimen they suggest is intense and will probably lead to overtraining in many people. They recommend resistance training major, multi-joint exercises, 1-3 sets to muscular failure 2-4 days a week. I've been at the higher end of that recommendation and it made my joints hurt, plus I was weaker than when I strength trained less frequently. I think the lower end of their recommendation, 1 set of each exercise to failure twice a week, is more than sufficient to meet the goal of maximizing improvements in body composition in most people. My current routine is one brief strength training session and one sprint session per week (in addition to my leisurely cycle commute), which works well for me on a cost-benefit level. However, I was stronger when I was strength training twice a week and never going to muscular failure (a la Pavel Tsatsouline).
Chapter 5, "Environment", is an interesting discussion of different factors that promote excessive calorie intake, such as the setting of the meal, the company or lack thereof, and food presentation. While they support their statements very well with evidence from scientific studies, I do have a lingering doubt about these types of studies: as far as I know, they're all based on short-term interventions. Science would be a lot easier if short-term always translated to long term, but unfortunately that's not the case. For example, studies lasting one or two weeks show that low glycemic index foods cause a reduction in calorie intake and greater feelings of fullness. However, this effect disappears in the long term, and numerous controlled trials show that low glycemic index diets have no effect on food intake, body weight or insulin sensitivity in the long term. I reviewed those studies here.
The body has homeostatic mechanisms (homeostatic = maintains the status quo) that regulate long-term energy balance. Whether short-term changes in calorie intake based on environmental cues would translate into sustained changes that would have a significant impact on body fat, I don't know. For example, if you eat a meal with your extended family at a restaurant that serves massive portions, you might eat twice as much as you would by yourself in your own home. But the question is, will your body factor that huge meal into your subsequent calorie intake and energy expenditure over the following days? The answer is clearly yes, but the degree of compensation is unclear. Since I'm not aware of any trials indicating that changing meal context can actually lead to long-term weight loss, I can't put much faith in this strategy (if you know otherwise, please link to the study in the comments).
Chapter 6, "Diet", is a very brief discussion of what to eat for weight loss. They basically recommend a low-calorie, low-carb diet focused on whole, natural foods. I think low-carbohydrate diets can be useful for some overweight people trying to lose weight, if for no other reason than the fact that they make it easier to control appetite. In addition, a subset of people respond very well to carbohydrate restriction in terms of body composition, health and well-being. The authors emphasize nutrient density, but don't really explain how to achieve it. It would have been nice to see a discussion of a few topics such as organ meats, leafy greens, dairy quality (pastured vs. conventional) and vitamin D. These may not help you lose weight, but they will help keep you healthy, particularly on a calorie-restricted diet. The authors also recommend a few energy bars, powders and supplements that I don't support. They state that they have no financial connection to the manufacturers of the products they recommend.
I'm wary of their recommendation to deliberately restrict calorie intake. Although it will clearly cause fat loss if you restrict calories enough, it's been shown to be ineffective for sustainable, long-term fat loss over and over again. The only exception is the rare person with an iron will who is able to withstand misery indefinitely. I'm going to keep an open mind on this question though. There may be a place for deliberate calorie restriction in the right context. But at this point I'm going to require some pretty solid evidence that it's effective, sustainable, and doesn't have unacceptable side effects.
The book contains a nice bonus, an appendix titled "What is Quality Evidence"? It's a brief discussion of common logical pitfalls when evaluating evidence, and I think many people could benefit from reading it.
Overall, S.P.E.E.D. was a worthwhile read, definitely superior to 95% of fat loss books. With some caveats mentioned above, I think it could be a useful resource for someone interested in fat loss.
Tuesday, October 19, 2010
Saturated Fat and Insulin Sensitivity
Insulin sensitivity is a measure of the tissue response to insulin. Typically, it refers to insulin's ability to cause tissues to absorb glucose from the blood. A loss of insulin sensitivity, also called insulin resistance, is a core part of the metabolic disorder that affects many people in industrial nations.
I don't know how many times I've seen the claim in journal articles and on the internet that saturated fat reduces insulin sensitivity. The idea is that saturated fat reduces the body's ability to handle glucose effectively, placing people on the road to diabetes, obesity and heart disease. Given the "selective citation disorder" that plagues the diet-health literature, perhaps this particular claim deserves a closer look.
The Evidence
I found a review article from 2008 that addressed this question (1). I like this review because it only includes high-quality trials that used reliable methods of determining insulin sensitivity*.
On to the meat of it. There were 5 studies in which non-diabetic people were fed diets rich in saturated fat, and compared with a group eating a diet rich in monounsaturated (like olive oil) or polyunsaturated (like corn oil) fat. They ranged in duration from one week to 3 months. Four of the five studies found that fat quality did not affect insulin sensitivity, including one of the 3-month studies.
The fifth study, which is the one that's nearly always cited in the diet-health literature, requires some discussion. This was the KANWU study (2). Over the course of three months, investigators fed 163 volunteers a diet rich in either saturated fat or monounsaturated fat.
What the authors decided to focus on instead is the fact that insulin sensitivity declined slightly but significantly on the saturated fat diet compared with the pre-diet baseline. That's why this study is cited as evidence that saturated fat impairs insulin sensitivity. But anyone who has a basic science background will see where this reasoning is flawed (warning: nerd attack. skip the rest of the paragraph if you're not interested). You need a control group for comparison, to take into account normal fluctuations caused by such things as the season, eating mostly cafeteria food, and having a doctor hooking you up to machines. That control group was the group eating monounsaturated fat. The comparison between diet groups was the 'primary outcome', in statistics lingo. That's the comparison that matters, and it wasn't significant. To interpret the study otherwise is to ignore the basic conventions of statistics, which the authors were happy to do. There's a name for it: 'moving the goalpost'. The reviewers shouldn't have let this kind of shenanigans slide.
So we have five studies through 2008, none of which support the idea that saturated fat reduces insulin sensitivity in non-diabetics. Since the review paper was published, I know of one subsequent study that asked the same question (3). Susan J. van Dijk and colleagues fed volunteers with abdominal overweight (beer gut) a diet rich in either saturated fat or monounsaturated fat. I e-mailed the senior author and she said the saturated fat diet was "mostly butter". The specific fats used in the diets weren't mentioned anywhere in the paper, which is a major omission**. In any case, after 8 weeks, insulin sensitivity was virtually identical between the two groups. This study appeared well controlled and used the gold standard method for assessing insulin sensitivity, called the euglycemic-hyperinsulinemic clamp technique***.
The evidence from controlled trials is rather consistent that saturated fat has no appreciable effect on insulin sensitivity.
Why Are We so Focused on Saturated Fat?
Answer: because it's the nutrient everyone loves to hate. As an exercise in completeness, I'm going to mention three dietary factors that actually reduce insulin sensitivity, and get a lot less air time than saturated fat.
#1: Caffeine. That's right, controlled trials show that your favorite murky beverage reduces insulin sensitivity (4, 5). Is it actually relevant to real life? I doubt it. The doses used were large and the studies short-term.
#2: Magnesium deficiency. A low-magnesium diet reduced insulin sensitivity by 25% over the course of three weeks (6). I think this is probably relevant to long-term insulin sensitivity and overall health, although it would be good to have longer-term data. Magnesium deficiency is widespread in industrial nations, due to our over-reliance on refined foods such as sugar, white flour and oils.
#3: Sugar. Fructose reduces insulin sensitivity in humans, along with many other harmful effects (7).
As long as we continue to focus our energy on indicting saturated fat, it will continue distracting us from the real causes of disease.
* For the nerds: euglycemic-hyperinsulinemic clamp (the gold standard), insulin suppression test, or intravenous glucose tolerance test with Minimal Model. They didn't include studies that reported HOMA as their only measure, because it's not very accurate.
** There's this idea that pervades the diet-health literature that all saturated fats are roughly equivalent, all monounsaturated fats are equivalent, etc., therefore it doesn't matter what the source was. This is beyond absurd and reflects our cultural obsession with saturated fat. It really irks me that the reviewers didn't demand this information.
*** They did find that markers of inflammation in fat tissue were higher after the saturated fat diet.
I don't know how many times I've seen the claim in journal articles and on the internet that saturated fat reduces insulin sensitivity. The idea is that saturated fat reduces the body's ability to handle glucose effectively, placing people on the road to diabetes, obesity and heart disease. Given the "selective citation disorder" that plagues the diet-health literature, perhaps this particular claim deserves a closer look.
The Evidence
I found a review article from 2008 that addressed this question (1). I like this review because it only includes high-quality trials that used reliable methods of determining insulin sensitivity*.
On to the meat of it. There were 5 studies in which non-diabetic people were fed diets rich in saturated fat, and compared with a group eating a diet rich in monounsaturated (like olive oil) or polyunsaturated (like corn oil) fat. They ranged in duration from one week to 3 months. Four of the five studies found that fat quality did not affect insulin sensitivity, including one of the 3-month studies.
The fifth study, which is the one that's nearly always cited in the diet-health literature, requires some discussion. This was the KANWU study (2). Over the course of three months, investigators fed 163 volunteers a diet rich in either saturated fat or monounsaturated fat.
The SAFA diet included butter and a table margarine containing a relatively high proportion of SAFAs. The MUFA diet included a spread and a margarine containing high proportions of oleic acid derived from high-oleic sunflower oil and negligible amounts of trans fatty acids and n-3 fatty acids and olive oil.Yummy. After three months of these diets, there was no significant difference in insulin sensitivity between the saturated fat group and the monounsaturated fat group. Yes, you read that right. Even the study that's selectively cited as evidence that saturated fat causes insulin resistance found no significant difference between the diets. You might not get this by reading the misleading abstract. I'll be generous and acknowledge that the (small) difference was almost statistically significant (p = 0.053).
What the authors decided to focus on instead is the fact that insulin sensitivity declined slightly but significantly on the saturated fat diet compared with the pre-diet baseline. That's why this study is cited as evidence that saturated fat impairs insulin sensitivity. But anyone who has a basic science background will see where this reasoning is flawed (warning: nerd attack. skip the rest of the paragraph if you're not interested). You need a control group for comparison, to take into account normal fluctuations caused by such things as the season, eating mostly cafeteria food, and having a doctor hooking you up to machines. That control group was the group eating monounsaturated fat. The comparison between diet groups was the 'primary outcome', in statistics lingo. That's the comparison that matters, and it wasn't significant. To interpret the study otherwise is to ignore the basic conventions of statistics, which the authors were happy to do. There's a name for it: 'moving the goalpost'. The reviewers shouldn't have let this kind of shenanigans slide.
So we have five studies through 2008, none of which support the idea that saturated fat reduces insulin sensitivity in non-diabetics. Since the review paper was published, I know of one subsequent study that asked the same question (3). Susan J. van Dijk and colleagues fed volunteers with abdominal overweight (beer gut) a diet rich in either saturated fat or monounsaturated fat. I e-mailed the senior author and she said the saturated fat diet was "mostly butter". The specific fats used in the diets weren't mentioned anywhere in the paper, which is a major omission**. In any case, after 8 weeks, insulin sensitivity was virtually identical between the two groups. This study appeared well controlled and used the gold standard method for assessing insulin sensitivity, called the euglycemic-hyperinsulinemic clamp technique***.
The evidence from controlled trials is rather consistent that saturated fat has no appreciable effect on insulin sensitivity.
Why Are We so Focused on Saturated Fat?
Answer: because it's the nutrient everyone loves to hate. As an exercise in completeness, I'm going to mention three dietary factors that actually reduce insulin sensitivity, and get a lot less air time than saturated fat.
#1: Caffeine. That's right, controlled trials show that your favorite murky beverage reduces insulin sensitivity (4, 5). Is it actually relevant to real life? I doubt it. The doses used were large and the studies short-term.
#2: Magnesium deficiency. A low-magnesium diet reduced insulin sensitivity by 25% over the course of three weeks (6). I think this is probably relevant to long-term insulin sensitivity and overall health, although it would be good to have longer-term data. Magnesium deficiency is widespread in industrial nations, due to our over-reliance on refined foods such as sugar, white flour and oils.
#3: Sugar. Fructose reduces insulin sensitivity in humans, along with many other harmful effects (7).
As long as we continue to focus our energy on indicting saturated fat, it will continue distracting us from the real causes of disease.
* For the nerds: euglycemic-hyperinsulinemic clamp (the gold standard), insulin suppression test, or intravenous glucose tolerance test with Minimal Model. They didn't include studies that reported HOMA as their only measure, because it's not very accurate.
** There's this idea that pervades the diet-health literature that all saturated fats are roughly equivalent, all monounsaturated fats are equivalent, etc., therefore it doesn't matter what the source was. This is beyond absurd and reflects our cultural obsession with saturated fat. It really irks me that the reviewers didn't demand this information.
*** They did find that markers of inflammation in fat tissue were higher after the saturated fat diet.
The Body Fat Setpoint, Part III: Dietary Causes of Obesity
What Caused the Setpoint to Change?
We have two criteria to narrow our search for the cause of modern fat gain:
In the last post, I described two mechanisms that may contribute to elevating the body fat set point by causing leptin resistance: inflammation in the hypothalamus, and impaired leptin transport into the brain due to elevated triglycerides. After more reading and discussing it with my mentor, I've decided that the triglyceride hypothesis is on shaky ground*. Nevertheless, it is consistent with certain observations:
The Role of Digestive Health
What causes inflammation in the hypothalamus? One of the most interesting hypotheses is that increased intestinal permeability allows inflammatory substances to cross into the circulation from the gut, irritating a number of tissues including the hypothalamus.
Dr. Remy Burcelin and his group have spearheaded this research. They've shown that high-fat diets cause obesity in mice, and that they also increase the level of an inflammatory substance called lipopolysaccharide (LPS) in the blood. LPS is produced by gram-negative bacteria in the gut and is one of the main factors that activates the immune system during an infection. Antibiotics that kill gram-negative bacteria in the gut prevent the negative consequences of high-fat feeding in mice.
Burcelin's group showed that infusing LPS into mice on a low-fat chow diet causes them to become obese and insulin resistant just like high-fat fed mice (4). Furthermore, adding 10% of the soluble fiber oligofructose to the high-fat diet prevented the increase in intestinal permeability and also largely prevented the body fat gain and insulin resistance from high-fat feeding (5). Oligofructose is food for friendly gut bacteria and ends up being converted to butyrate and other short-chain fatty acids in the colon. This results in lower intestinal permeability to toxins such as LPS. This is particularly interesting because oligofructose supplements cause fat loss in humans (6).
A recent study showed that blood LPS levels are correlated with body fat, elevated cholesterol and triglycerides, and insulin resistance in humans (7). However, a separate study didn't come to the same conclusion (8). The discrepancy may be due to the fact that LPS isn't the only inflammatory substance to cross the gut lining-- other substances may also be involved. Anything in the blood that shouldn't be there is potentially inflammatory.
Overall, I think gut dysfunction probably plays a major role in obesity and other modern metabolic problems. Insufficient dietary fiber, micronutrient deficiencies, excessive gut irritating substances such as gluten, abnormal bacterial growth due to refined carbohydrates (particularly sugar), and omega-6:3 imbalance may all contribute to abnormal gut bacteria and increased gut permeability.
The Role of Fatty Acids and Micronutrients
Any time a disease involves inflammation, the first thing that comes to my mind is the balance between omega-6 and omega-3 fats. The modern Western diet is heavily weighted toward omega-6, which are the precursors to some very inflammatory substances (as well as a few that are anti-inflammatory). These substances are essential for health in the correct amounts, but they need to be balanced with omega-3 to prevent excessive and uncontrolled inflammatory responses. Animal models have repeatedly shown that omega-3 deficiency contributes to the fat gain and insulin resistance they develop when fed high-fat diets (9, 10, 11).
As a matter of fact, most of the papers claiming "saturated fat causes this or that in rodents" are actually studying omega-3 deficiency. The "saturated fats" that are typically used in high-fat rodent diets are refined fats from conventionally raised animals, which are very low in omega-3. If you add a bit of omega-3 to these diets, suddenly they don't cause the same metabolic problems, and are generally superior to refined seed oils, even in rodents (12, 13).
I believe that micronutrient deficiency also plays a role. Inadequate vitamin and mineral status can contribute to inflammation and weight gain. Obese people typically show deficiencies in several vitamins and minerals. The problem is that we don't know whether the deficiencies caused the obesity or vice versa. Refined carbohydrates and refined oils are the worst offenders because they're almost completely devoid of micronutrients.
Vitamin D in particular plays an important role in immune responses (including inflammation), and also appears to influence body fat mass. Vitamin D status is associated with body fat and insulin sensitivity in humans (14, 15, 16). More convincingly, genetic differences in the vitamin D receptor gene are also associated with body fat mass (17, 18), and vitamin D intake predicts future fat gain (19).
Exiting the Niche
I believe that we have strayed too far from our species' ecological niche, and our health is suffering. One manifestation of that is body fat gain. Many factors probably contribute, but I believe that diet is the most important. A diet heavy in nutrient-poor refined carbohydrates and industrial omega-6 oils, high in gut irritating substances such as gluten and sugar, and a lack of direct sunlight, have caused us to lose the robust digestion and good micronutrient status that characterized our distant ancestors. I believe that one consequence has been the dysregulation of the system that maintains the fat mass "setpoint". This has resulted in an increase in body fat in 20th century affluent nations, and other cultures eating our industrial food products.
In the next post, I'll discuss my thoughts on how to reset the body fat setpoint.
* The ratio of leptin in the serum to leptin in the brain is diminished in obesity, but given that serum leptin is very high in the obese, the absolute level of leptin in the brain is typically not lower than a lean person. Leptin is transported into the brain by a transport mechanism that saturates when serum leptin is not that much higher than the normal level for a lean person. Therefore, the fact that the ratio of serum to brain leptin is higher in the obese does not necessarily reflect a defect in transport, but rather the fact that the mechanism that transports leptin is already at full capacity.
We have two criteria to narrow our search for the cause of modern fat gain:
- It has to be new to the human environment
- It has to cause leptin resistance or otherwise disturb the setpoint
In the last post, I described two mechanisms that may contribute to elevating the body fat set point by causing leptin resistance: inflammation in the hypothalamus, and impaired leptin transport into the brain due to elevated triglycerides. After more reading and discussing it with my mentor, I've decided that the triglyceride hypothesis is on shaky ground*. Nevertheless, it is consistent with certain observations:
- Fibrate drugs that lower triglycerides can lower fat mass in rodents and humans
- Low-carbohydrate diets are effective for fat loss and lower triglycerides
- Fructose can cause leptin resistance in rodents and it elevates triglycerides (1)
- Fish oil reduces triglycerides. Some but not all studies have shown that fish oil aids fat loss (2)
The Role of Digestive Health
What causes inflammation in the hypothalamus? One of the most interesting hypotheses is that increased intestinal permeability allows inflammatory substances to cross into the circulation from the gut, irritating a number of tissues including the hypothalamus.
Dr. Remy Burcelin and his group have spearheaded this research. They've shown that high-fat diets cause obesity in mice, and that they also increase the level of an inflammatory substance called lipopolysaccharide (LPS) in the blood. LPS is produced by gram-negative bacteria in the gut and is one of the main factors that activates the immune system during an infection. Antibiotics that kill gram-negative bacteria in the gut prevent the negative consequences of high-fat feeding in mice.
Burcelin's group showed that infusing LPS into mice on a low-fat chow diet causes them to become obese and insulin resistant just like high-fat fed mice (4). Furthermore, adding 10% of the soluble fiber oligofructose to the high-fat diet prevented the increase in intestinal permeability and also largely prevented the body fat gain and insulin resistance from high-fat feeding (5). Oligofructose is food for friendly gut bacteria and ends up being converted to butyrate and other short-chain fatty acids in the colon. This results in lower intestinal permeability to toxins such as LPS. This is particularly interesting because oligofructose supplements cause fat loss in humans (6).
A recent study showed that blood LPS levels are correlated with body fat, elevated cholesterol and triglycerides, and insulin resistance in humans (7). However, a separate study didn't come to the same conclusion (8). The discrepancy may be due to the fact that LPS isn't the only inflammatory substance to cross the gut lining-- other substances may also be involved. Anything in the blood that shouldn't be there is potentially inflammatory.
Overall, I think gut dysfunction probably plays a major role in obesity and other modern metabolic problems. Insufficient dietary fiber, micronutrient deficiencies, excessive gut irritating substances such as gluten, abnormal bacterial growth due to refined carbohydrates (particularly sugar), and omega-6:3 imbalance may all contribute to abnormal gut bacteria and increased gut permeability.
The Role of Fatty Acids and Micronutrients
Any time a disease involves inflammation, the first thing that comes to my mind is the balance between omega-6 and omega-3 fats. The modern Western diet is heavily weighted toward omega-6, which are the precursors to some very inflammatory substances (as well as a few that are anti-inflammatory). These substances are essential for health in the correct amounts, but they need to be balanced with omega-3 to prevent excessive and uncontrolled inflammatory responses. Animal models have repeatedly shown that omega-3 deficiency contributes to the fat gain and insulin resistance they develop when fed high-fat diets (9, 10, 11).
As a matter of fact, most of the papers claiming "saturated fat causes this or that in rodents" are actually studying omega-3 deficiency. The "saturated fats" that are typically used in high-fat rodent diets are refined fats from conventionally raised animals, which are very low in omega-3. If you add a bit of omega-3 to these diets, suddenly they don't cause the same metabolic problems, and are generally superior to refined seed oils, even in rodents (12, 13).
I believe that micronutrient deficiency also plays a role. Inadequate vitamin and mineral status can contribute to inflammation and weight gain. Obese people typically show deficiencies in several vitamins and minerals. The problem is that we don't know whether the deficiencies caused the obesity or vice versa. Refined carbohydrates and refined oils are the worst offenders because they're almost completely devoid of micronutrients.
Vitamin D in particular plays an important role in immune responses (including inflammation), and also appears to influence body fat mass. Vitamin D status is associated with body fat and insulin sensitivity in humans (14, 15, 16). More convincingly, genetic differences in the vitamin D receptor gene are also associated with body fat mass (17, 18), and vitamin D intake predicts future fat gain (19).
Exiting the Niche
I believe that we have strayed too far from our species' ecological niche, and our health is suffering. One manifestation of that is body fat gain. Many factors probably contribute, but I believe that diet is the most important. A diet heavy in nutrient-poor refined carbohydrates and industrial omega-6 oils, high in gut irritating substances such as gluten and sugar, and a lack of direct sunlight, have caused us to lose the robust digestion and good micronutrient status that characterized our distant ancestors. I believe that one consequence has been the dysregulation of the system that maintains the fat mass "setpoint". This has resulted in an increase in body fat in 20th century affluent nations, and other cultures eating our industrial food products.
In the next post, I'll discuss my thoughts on how to reset the body fat setpoint.
* The ratio of leptin in the serum to leptin in the brain is diminished in obesity, but given that serum leptin is very high in the obese, the absolute level of leptin in the brain is typically not lower than a lean person. Leptin is transported into the brain by a transport mechanism that saturates when serum leptin is not that much higher than the normal level for a lean person. Therefore, the fact that the ratio of serum to brain leptin is higher in the obese does not necessarily reflect a defect in transport, but rather the fact that the mechanism that transports leptin is already at full capacity.
The Dirty Little Secret of the Diet-Heart Hypothesis
The diet-heart hypothesis is the idea that saturated fat, and in some versions cholesterol, raises blood cholesterol and contributes to the risk of having a heart attack. To test this hypothesis, scientists have been studying the relationship between saturated fat consumption and heart attack risk for more than half a century. To judge by the grave pronouncements of our most visible experts, you would think these studies had found an association between the two. It turns out, they haven't.
The fact is, the vast majority of high-quality observational studies have found no connection whatsoever between saturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the squirming about saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Don't let the abstract fool you! Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. This one fooled me for a long time because the abstract is misleading. It claims that saturated fat was associated with heart attack risk. However, the association disappeared without a trace when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is anywhere near as harmful as we're told, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be fair, there have been a few that have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was minuscule.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. If this substance is truly so fearsome, why don't people who eat more of it have more heart attacks? In case you're concerned that I'm cherry-picking studies that conform to my beliefs, here are links to review papers on the same data that have reached the same conclusion:
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov systematically demolishes the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association whatsoever between saturated fat consumption and heart attack risk.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. This is held as established fact in the mainstream understanding of nutrition. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol. The association between blood cholesterol and heart attack risk does not apply to Japanese populations, as pointed out repeatedly by the erudite Dr. Harumi Okuyama. This seems to be generally true of groups that consume a lot of seafood.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. This turns out to be largely a myth, based on a liberal interpretation of short-term feeding studies. In fact, it isn't even true in animal models of heart disease. In the 1950s, the most vigorous proponent of the diet-heart hypothesis, Dr. Ancel Keys, created a formula designed to predict changes in blood cholesterol based on the consumption of dietary saturated and polyunsaturated fats. This formula is extremely inaccurate and has gradually been dropped from the modern medical literature. Yet the idea that saturated fat consumption increases blood cholesterol/LDL lives on...
This is it, folks: the diet-heart hypothesis ends here. It's been kept afloat for decades by wishful thinking, puritan sensibilities and selective citation of the evidence. It's time to put it out of its misery.
The fact is, the vast majority of high-quality observational studies have found no connection whatsoever between saturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the squirming about saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Don't let the abstract fool you! Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. This one fooled me for a long time because the abstract is misleading. It claims that saturated fat was associated with heart attack risk. However, the association disappeared without a trace when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is anywhere near as harmful as we're told, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be fair, there have been a few that have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was minuscule.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. If this substance is truly so fearsome, why don't people who eat more of it have more heart attacks? In case you're concerned that I'm cherry-picking studies that conform to my beliefs, here are links to review papers on the same data that have reached the same conclusion:
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov systematically demolishes the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association whatsoever between saturated fat consumption and heart attack risk.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. This is held as established fact in the mainstream understanding of nutrition. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol. The association between blood cholesterol and heart attack risk does not apply to Japanese populations, as pointed out repeatedly by the erudite Dr. Harumi Okuyama. This seems to be generally true of groups that consume a lot of seafood.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. This turns out to be largely a myth, based on a liberal interpretation of short-term feeding studies. In fact, it isn't even true in animal models of heart disease. In the 1950s, the most vigorous proponent of the diet-heart hypothesis, Dr. Ancel Keys, created a formula designed to predict changes in blood cholesterol based on the consumption of dietary saturated and polyunsaturated fats. This formula is extremely inaccurate and has gradually been dropped from the modern medical literature. Yet the idea that saturated fat consumption increases blood cholesterol/LDL lives on...
This is it, folks: the diet-heart hypothesis ends here. It's been kept afloat for decades by wishful thinking, puritan sensibilities and selective citation of the evidence. It's time to put it out of its misery.
Monday, May 24, 2010
Thank You
I'd like to extend my sincere thanks to everyone who has supported me through donations this year. The money has allowed me to buy materials that I wouldn't otherwise have been able to afford, and I feel it has enriched the blog for everyone. Here are some of the books I've bought using donations. Some were quite expensive:
Food and western disease: health and nutrition from an evolutionary perspective. Staffan Lindeberg (just released!!)
Nutrition and disease. Edward Mellanby
Migration and health in a small society: the case of Tokelau. Edited by Albert F. Wessen
The saccharine disease. T. L. Cleave
Culture, ecology and dental anthropology. John R. Lukacs
Vitamin K in health and disease. John W. Suttie
Craniofacial development. Geoffrey H. Sperber
Western diseases: their emergence and prevention. Hugh C. Trowell and Denis P. Burkitt
The ultimate omega-3 diet. Evelyn Tribole
Our changing fare. John Yudkin and colleagues
Donations have also paid for many, many photocopies at the medical library. I'd also like to thank everyone who participates in the community by leaving comments, or by linking to my posts. I appreciate your encouragement, and also the learning opportunities.
Food and western disease: health and nutrition from an evolutionary perspective. Staffan Lindeberg (just released!!)
Nutrition and disease. Edward Mellanby
Migration and health in a small society: the case of Tokelau. Edited by Albert F. Wessen
The saccharine disease. T. L. Cleave
Culture, ecology and dental anthropology. John R. Lukacs
Vitamin K in health and disease. John W. Suttie
Craniofacial development. Geoffrey H. Sperber
Western diseases: their emergence and prevention. Hugh C. Trowell and Denis P. Burkitt
The ultimate omega-3 diet. Evelyn Tribole
Our changing fare. John Yudkin and colleagues
Donations have also paid for many, many photocopies at the medical library. I'd also like to thank everyone who participates in the community by leaving comments, or by linking to my posts. I appreciate your encouragement, and also the learning opportunities.
Magnesium and Insulin Sensitivity
From a paper based on US NHANES nutrition and health survey data (1):
Magnesium status is associated with insulin sensitivity (2, 3), and a low magnesium intake predicts the development of type II diabetes in most studies (4, 5) but not all (6). Magnesium supplements largely prevent diabetes in a rat model* (7). Interestingly, excess blood glucose and insulin themselves seem to reduce magnesium status, possibly creating a vicious cycle.
In a 1993 trial, a low-magnesium diet reduced insulin sensitivity in healthy volunteers by 25% in just four weeks (8). It also increased urinary thromboxane concentration, a potential concern for cardiovascular health**.
At least three trials have shown that magnesium supplementation increases insulin sensitivity in insulin-resistant diabetics and non-diabetics (9, 10, 11). In some cases, the results were remarkable. In type II diabetics, 16 weeks of magnesium supplementation improved fasting glucose, calculated insulin sensitivity and HbA1c*** (12). HbA1c dropped by 22 percent.
In insulin resistant volunteers with low blood magnesium, magnesium supplementation for four months reduced estimated insulin resistance by 43 percent and decreased fasting insulin by 32 percent (13). This suggests to me that magnesium deficiency was probably one of the main reasons they were insulin resistant in the first place. But the study had another very interesting finding: magnesium improved the subjects' blood lipid profile remarkably. Total cholesterol decreased, LDL decreased, HDL increased and triglycerides decreased by a whopping 39 percent. The same thing had been reported in the medical literature decades earlier when doctors used magnesium injections to treat heart disease, and also in animals treated with magnesium. Magnesium supplementation also suppresses atherosclerosis (thickening and hardening of the arteries) in animal models, a fact that I may discuss in more detail at some point (14, 15).
In the previous study, participants were given 2.5 g magnesium chloride (MgCl2) per day. That's a bit more than the USDA recommended daily allowance (MgCl2 is mostly chloride by weight), in addition to what they were already getting from their diet. Most of a person's magnesium is in their bones, so correcting a deficiency by eating a nutritious diet may take a while.
Speaking of nutritious diets, how does one get magnesium? Good sources include halibut, leafy greens, chocolate and nuts. Bone broths are also an excellent source of highly absorbable magnesium. Whole grains and beans are also fairly good sources, while refined grains lack most of the magnesium in the whole grain. Organic foods, particularly artisanally produced foods from a farmer's market, are richer in magnesium because they grow on better soil and often use older varieties that are more nutritious.
The problem with seeds such as grains, beans and nuts is that they also contain phytic acid which prevents the absorption of magnesium and other minerals (16). Healthy non-industrial societies that relied on grains took great care in their preparation: they soaked them, often fermented them, and also frequently removed a portion of the bran before cooking (17). These steps all served to reduce the level of phytic acid and other anti-nutrients. I've posted a method for effectively reducing the amount of phytic acid in brown rice (18). Beans should ideally be soaked for 24 hours before cooking, preferably in warm water.
Industrial agriculture has systematically depleted our soil of many minerals, due to high-yield crop varieties and the fact that synthetic fertilizers only replace a few minerals. The mineral content of foods in the US, including magnesium, has dropped sharply in the last 50 years. The reason we need to use fertilizers in the first place is that we've broken the natural nutrient cycle in which minerals always return to the soil in the same place they were removed. In 21st century America, minerals are removed from the soil, pass through our toilets, and end up in the landfill or in waste water. This will continue until we find an acceptable way to return human feces and urine to agricultural soil, as many cultures do to this day****.
I believe that an adequate magnesium intake is critical for proper insulin sensitivity and overall health.
* Zucker rats that lack leptin signaling
** Thromboxane A2 is an omega-6 derived eicosanoid that potently constricts blood vessels and promotes blood clotting. It's interesting that magnesium has such a strong effect on it. It indicates that fatty acid balance is not the only major influence on eicosanoid production.
*** Glycated hemoglobin. A measure of the average blood glucose level over the past few weeks.
**** Anyone interested in further reading on this should look up The Humanure Handbook
During 1999–2000, the diet of a large proportion of the U.S. population did not contain adequate magnesium... Furthermore, racial or ethnic differences in magnesium persist and may contribute to some health disparities.... Because magnesium intake is low among many people in the United States and inadequate magnesium status is associated with increased risk of acute and chronic conditions, an urgent need exists to perform a current survey to assess the physiologic status of magnesium in the U.S. population.Magnesium is an essential mineral that's slowly disappearing from the modern diet, as industrial agriculture and industrial food processing increasingly dominate our food choices. One of the many things it's necessary for in mammals is proper insulin sensitivity and glucose control. A loss of glucose control due to insulin resistance can eventually lead to diabetes and all its complications.
Magnesium status is associated with insulin sensitivity (2, 3), and a low magnesium intake predicts the development of type II diabetes in most studies (4, 5) but not all (6). Magnesium supplements largely prevent diabetes in a rat model* (7). Interestingly, excess blood glucose and insulin themselves seem to reduce magnesium status, possibly creating a vicious cycle.
In a 1993 trial, a low-magnesium diet reduced insulin sensitivity in healthy volunteers by 25% in just four weeks (8). It also increased urinary thromboxane concentration, a potential concern for cardiovascular health**.
At least three trials have shown that magnesium supplementation increases insulin sensitivity in insulin-resistant diabetics and non-diabetics (9, 10, 11). In some cases, the results were remarkable. In type II diabetics, 16 weeks of magnesium supplementation improved fasting glucose, calculated insulin sensitivity and HbA1c*** (12). HbA1c dropped by 22 percent.
In insulin resistant volunteers with low blood magnesium, magnesium supplementation for four months reduced estimated insulin resistance by 43 percent and decreased fasting insulin by 32 percent (13). This suggests to me that magnesium deficiency was probably one of the main reasons they were insulin resistant in the first place. But the study had another very interesting finding: magnesium improved the subjects' blood lipid profile remarkably. Total cholesterol decreased, LDL decreased, HDL increased and triglycerides decreased by a whopping 39 percent. The same thing had been reported in the medical literature decades earlier when doctors used magnesium injections to treat heart disease, and also in animals treated with magnesium. Magnesium supplementation also suppresses atherosclerosis (thickening and hardening of the arteries) in animal models, a fact that I may discuss in more detail at some point (14, 15).
In the previous study, participants were given 2.5 g magnesium chloride (MgCl2) per day. That's a bit more than the USDA recommended daily allowance (MgCl2 is mostly chloride by weight), in addition to what they were already getting from their diet. Most of a person's magnesium is in their bones, so correcting a deficiency by eating a nutritious diet may take a while.
Speaking of nutritious diets, how does one get magnesium? Good sources include halibut, leafy greens, chocolate and nuts. Bone broths are also an excellent source of highly absorbable magnesium. Whole grains and beans are also fairly good sources, while refined grains lack most of the magnesium in the whole grain. Organic foods, particularly artisanally produced foods from a farmer's market, are richer in magnesium because they grow on better soil and often use older varieties that are more nutritious.
The problem with seeds such as grains, beans and nuts is that they also contain phytic acid which prevents the absorption of magnesium and other minerals (16). Healthy non-industrial societies that relied on grains took great care in their preparation: they soaked them, often fermented them, and also frequently removed a portion of the bran before cooking (17). These steps all served to reduce the level of phytic acid and other anti-nutrients. I've posted a method for effectively reducing the amount of phytic acid in brown rice (18). Beans should ideally be soaked for 24 hours before cooking, preferably in warm water.
Industrial agriculture has systematically depleted our soil of many minerals, due to high-yield crop varieties and the fact that synthetic fertilizers only replace a few minerals. The mineral content of foods in the US, including magnesium, has dropped sharply in the last 50 years. The reason we need to use fertilizers in the first place is that we've broken the natural nutrient cycle in which minerals always return to the soil in the same place they were removed. In 21st century America, minerals are removed from the soil, pass through our toilets, and end up in the landfill or in waste water. This will continue until we find an acceptable way to return human feces and urine to agricultural soil, as many cultures do to this day****.
I believe that an adequate magnesium intake is critical for proper insulin sensitivity and overall health.
* Zucker rats that lack leptin signaling
** Thromboxane A2 is an omega-6 derived eicosanoid that potently constricts blood vessels and promotes blood clotting. It's interesting that magnesium has such a strong effect on it. It indicates that fatty acid balance is not the only major influence on eicosanoid production.
*** Glycated hemoglobin. A measure of the average blood glucose level over the past few weeks.
**** Anyone interested in further reading on this should look up The Humanure Handbook
How to Review Your Homeowners Insurance Renewal Statement
For most of us, our home is our single largest and most important investment. Many of us have poured thousands of dollars and countless hours into maintaining, improving and (hopefully) paying off our homes. Many people own their homes free of any mortgage. These assets are pure equity. Certainly its worthwhile to invest 15 minutes a year to be sure it's properly insured.
Thankfully, the insurance company offers you a perfect reminder and opportunity in sending out your annual renewal statement. Even if your insurance is paid by your mortgage company as part of your impound account, the insurance company still mails you a statement of renewal every year to update you with your current coverage limits and deductible.
Here's a few important steps you can take to be sure that HOME SWEET HOME is properly protected.
1. Check the basics. Check your name, address and any other description of the insured property. Make sure there's been no change of vesting or ownership that needs to be updated. Check your address to be sure no numbers are transposed.
2. Check the mortgagee clause. Here's where you can be sure that the current mortagee on your home is listed correctly. Check the lender, address and your loan number. Be sure there's no old information there. Maybe you had a HELOC (Home Equity Line of Credit) or a second mortgage that no longer applies. Be sure to get them removed.
Thankfully, the insurance company offers you a perfect reminder and opportunity in sending out your annual renewal statement. Even if your insurance is paid by your mortgage company as part of your impound account, the insurance company still mails you a statement of renewal every year to update you with your current coverage limits and deductible.
Here's a few important steps you can take to be sure that HOME SWEET HOME is properly protected.
1. Check the basics. Check your name, address and any other description of the insured property. Make sure there's been no change of vesting or ownership that needs to be updated. Check your address to be sure no numbers are transposed.
2. Check the mortgagee clause. Here's where you can be sure that the current mortagee on your home is listed correctly. Check the lender, address and your loan number. Be sure there's no old information there. Maybe you had a HELOC (Home Equity Line of Credit) or a second mortgage that no longer applies. Be sure to get them removed.
HEADS UP: Whenever you have a significant claim, the mortgage company will be one of the payees on your claim settlement check. Just that alone can be an inconvenience. But it becomes a major hassle when one of the institutions listed no longer has a vested interest in your home. The insurance company is bound by contract to include the mortgage company on all settlement checks beyond a stated threshold.
*3. Check the coverage on your home (dwelling or building). This is without question the single most important coverage to examine, consider and adjust whenever necessary. Having been an agent during the two raging firestorms in San Diego, CA in this decade, I can tell you that underinsured homes are just NO FUN! Two of my clients lost their homes in the 2003 fires and fortunately they were both adequately insured. (we call all our homeowner clients once a year to review their coverages and suggest improvements and adjustments) But I can tell you that there were literally hundreds of people in the area that were not so fortunate. Many were underinsured by over $100,000! Contractors were giving rebuilding bids on homes for $400,000 with insurance policies with limits less than $300,000. See if that doesn't tweak your financial well-being just a little. Here's the solution.Get an accurate rendering of the square footage of your home. Check county records, take a look at zillow.com, call your favorite Realtor, or get a tape measure and do your thing. Usually you don't include the garage in this calculation. Once you get your square footage, then you need to determine the building cost per square foot in your area for a home like yours. Call a local contractor for a quick estimate or you can call your insurance agent. Average costs in San Diego run about $200 per square foot. With that, a 2000 square foot would take about $400,000 to rebuild. Custom homes can be significantlly more. For a more complete discussion of this, check out: How Much Homeowners Insurance Do You REALLY Need?
Your contents coverage is usually 75% of the amount you have on your home. For example, if you have $400,000 on your home, you'll have an additional $300,000 to cover your personal property (furniture, clothing, dishes, TV, collections, shoes, tools, etc) Usually this is enough, but think through it anyway. If you have antiques, art, collections of any kind then you may need more. Ask your agent for help if you need to.
4. Look at your Personal Liability Coverage. This is the coverage you need when you get sued. Little Johnny runs across your front yard and trips on one of your sprinklers and ruins his chances to become America's Next Top Model and his parents sue your for $250,000. Make sure you don't scrimp here. It's not too expensive to get $500,000 or even $1 Million of liability coverage. If you have $100,000 or less, you could be setting yourself up for a mess just waiting to happen. Put a really big checkbook between your assets and someone who sees an injury as a lifetime paycheck. You might even consider a Liability Umbrella.
5. Check your 'special limits'. This is a REALLY BROAD subject that I just can't do justice to here in this post. Simply stated, there's limits on many things such as cash, computers, cameras, jewelry, furs, goldware, silverware, tools, etc. Call your company and ask for a review. You can increase many of these limits for just a few dollars a year. Sometimes the available increase isn't enough. That's the perfect time to consider a Personal Articles Floater (or it's called many different names) It's a policy that's designed to place stated amounts of coverage on many items from jewelry, business tools, iPods, hearing aids, cameras, musical instruments and on and on. If you have more than 'the average Joe' of ANYTHING, then check this out FOR SURE!
6. Check your deductible! This can be a tremendous cost-control tool in your insurance spending. Simply stated: The larger your deductible, the greater your savings. Usually you can save close to $100 per year just by going from a $500 deductible to $1000. Pick the largest number you can stand without losing sleep at night and ask your agent or company the savings you'd realize by changing. If you have a $250 or smaller deductible, it's definitely time to change it UP! Keep in mind that you usually hit a point of 'diminishing returns' once you get to $4000 or more. This means that you'll save less and less for each additional $1000 you choose. It might make sense to go from $1000 to $2000 if you save $85 a year by doing so, but not from $5000 to $6000 if you only save another $21 by making that jump.
Monitoring your insurance costs and coverages can result in a lot of savings AND peace of mind. Be sure you keep notes and file your thoughts and changes from year to year. These recoreds will make your annual call quicker and easier each year.
Feel free to contact me anytime if you have questions.
Till next time...
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