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.

Dr. Rosedale Replies

A few months ago, I posted link to an article by Dr. Ron Rosedale and made a few comments about it. Dr. Rosedale has sent a reply to my comments, which I have agreed to publish as a new post because they may be of interest to readers. In the following exchange, my numbered comments are in quotes and Dr. Rosedale's replies follow them.

Dr. Rosedale's Comments

1. Dr. Rosedale says that insulin's ability to regulate blood sugar is a minor role, and that other hormones do the same thing. Tell that to a type 1 diabetic. Excessive blood glucose is Not Good, and that's what you get if there isn't enough insulin around.

What I have said was that insulin does not control glucose levels in the blood, and that insulin's biological purpose (not ability) plays only a minor role in BS control... and that is a correct statement. Insulin reduces blood glucose by storing it for a rainy day as glycogen and fat, but not for the purpose of regulating blood sugar levels. The control of BS is in an upward direction, not a downward direction. The problem in our evolutionary history was to have enough BS for emergency anaerobic respiration and for those tissues that require it such as red blood cells. Lowering blood sugar was never a priority in our history. For one, it didn't rise much very often. There wasn't much glucose around. Uncooked rice and potatoes, etc., are mostly indigestible. The sugar that was around, such as in fruit, required considerable effort to obtain therefore lowered the sugar prior to obtaining it. Also, the sugar that is in fruit is largely fructose which doesn't convert that much into glucose but rather into fat in the liver. Even if it did raise blood sugar levels, even if it did cause diabetes in evolutionary time, nature would consider that irrelevant as it wouldn't have killed people prior to the reproductive years, only post-reproductively when nature doesn't give a damn.

Furthermore, insulin's major purpose goes way beyond sugar. At the very least, it is a nutrient storage hormone being relevant not only in glucose storage, but also in fat and protein (amino acid) storage. It also plays a significant role in micronutrient storage and conversions. However, overwhelmingly more important, is insulin's role as a nutrient sensor greatly influencing genetic expression and modifying the rate of aging by up or down regulating maintenance and repair.

2. I'm not convinced by the theory that organisms balance reproduction and repair, emphasizing one at the expense of the other. The amount of energy it takes to fuel cellular repair processes is negligible compared to the amount it takes to maintain body temperature, fuel the brain and contract skeletal muscles. Why not just have the organism eat an extra half-teaspoon of mashed potatoes to fuel the heat-shock proteins and make a little extra catalase? I think the true reasons behind lifespan extension upon caloric restriction will turn out to be more complex than a balance between reproduction and repair.

Stephan does not have to be convinced. Almost everybody who studies the biology of aging is convinced that there is a dichotomy between reproduction and maintenance and repair and that biologically a cell can spend the majority of available resources towards one or the other, but not both. This can actually be shown genetically as the up or down regulation of the expression of genes regulating heat shock proteins, intracellular antioxidant systems, DNA repair enzymes, "garbage collection", etc versus the up or down regulation of genes which regulate reproductive behavior. It should also be noted that excessive reproductive behavior is, in individual cells of multicellular organisms, a strong predisposition to cancer. Furthermore, Stephan’s statement that it takes negligible energy for maintenance and repair is very wrong. In fact one could make the argument that almost all of the energy spent by both individual cells and by the cell societies of multi-celled organisms when not reproducing is towards maintenance and repair.

3. I disagree with the idea that carbohydrate itself is behind elevated fasting insulin and leptin. Just look at the Kitavans. They get 69% of their calories from high-glycemic-load carbohydrates, with not much fat (21%) or protein (10%) to slow digestion. Yet, they have low fasting insulin and remarkably low fasting leptin. I believe the fasting levels of these hormones are more responsive to macronutrient quality than quantity. In other words, what matters most is not how much carbohydrate is in the diet, but where the carbohydrate comes from. The modern Western combination of carelessly processed wheat, sugar and linoleic acid-rich vegetable oil seems to be particularly harmful.

It is not where the carbohydrates come from, but where the carbohydrates go. In other words, what carbohydrates are digested into, i.e what the cells are being fed. Feeding them glucose, fructose, galactose and amino acids as energy (as opposed to using the amino acids whole as structural components) is bad.

Stephan himself could answer this one. It's not the percent of calories from carbohydrates that is relevant; it is the absolute amount of non-fiber carbohydrates that is relevant as the glycemic load.

A few further comments on the Kitavans, though I really am not an expert on their diet:

I find that indigenous diets are only partially helpful as there are so many variables that can go unaccounted for. I prefer the more elementary sciences to form opinions. However, it sounds like there really isn't that much non-fiber carbohydrate in the diet and there is considerable fiber, fish and coconut oil, and moderate to low protein, all of which are quite fine for health. If it is known, the total gram quantities of macronutrients would be good to know. Another important point; what is their lifespan? It sounds like it might be long, but it would be nice to know a more accurate figure. It is not weight loss that we should be after, it is health as indicated by a long and youthful lifespan. Another point; though they (the Kitavans) may be doing well if one defines well as better than most human counterparts, it isn't really saying much. The majority of society eats so badly that it really is not difficult to eat a diet that is better. What I am after is not just better, but best. Perhaps one could take the Kitavan diet and improve upon it by reducing the non-fiber carbohydrate content and perhaps adding more beneficial fats and oils. It is quite possible, in fact probable, that there have been no human societies that have eaten an ideal diet. We can only use what modern science is telling us to come up with this.

My Reply to Dr. Rosedale

Thank you for your comments.

1. I agree with you that control of blood sugar is not insulin's only purpose, and that there are other mechanisms of blood glucose control. There were several papers published recently showing that type 1 diabetic rats (lacking insulin) can be restored to a normal blood glucose level and near-normal glucose tolerance by infusing leptin into the lateral or the third cerebral ventricles (1, 2). This was totally independent of insulin, because the rats weren't producing any. And yes, insulin signaling influences lifespan in a number of animal models.

However, insulin is still the primary controller of blood sugar under normal circumstances, as shown in type 1 diabetes where the primary defect is in insulin production. Furthermore, excessively elevated glucose is damaging per se, due to protein glycation, competition with vitamin C, etc. Therefore, the glucose-controlling function of insulin is important.

I do not agree that glucose from starch and fruit played an insignificant role in human evolution. A number of modern hunter-gatherers eat a significant amount of starch, and our ancestors probably did as well, as soon as they could cook. The timeline of cooking is debated, but we've probably been doing it for at least half a million years, or as long as Homo sapiens has existed. Fruit sugar is roughly 50% glucose, as is honey.

2. As someone who spent two years in the field of aging research, I don't see a scientific consensus on the idea that reproduction and aging are in balance with one another. The two correlate with one another in some, but not all models. I was at a seminar just the other day by Dr. Linda Partridge, from the Max Planck institute, and she was talking about her lifespan experiments in fruit flies. She was able to independently modify lifespan and fecundity using amino acid restriction, leading her to the conclusion that there is no link between the two in her model. She published these data recently in the journal Nature (reference).

Regarding the energy required for cellular maintenance, a little math is instructive here. I eat maybe 3,200 calories a day, which is normal for an active male of my weight. My basal metabolic rate is roughly 1,700 kcal per day. So 1,500 of my calories have already gone to moving my skeletal muscles. Of the basal metabolic rate, the vast majority comes from maintaining body temperature. Thermogenesis is why cold-blooded animals only need to eat a fraction of the calories mammals do. Then there's cardiac function, and smooth muscle activity, which eat up more calories. Then there are the energy-intensive cellular processes of maintaining ionic gradients across cell membranes (which is why the brain eats up 20% of our calories) and protein synthesis.

After you subtract out all those functions, only a small fraction of total caloric intake is left for other cellular processes. So the caloric needs for processes that combat cellular aging (DNA repair, etc.) are quite low, compared to overall energy requirements. This is consistent with the fact that naked mole rats, which live ten times longer than Rattus norvegicus, have a similar basal metabolic rate to one another. Keeping cells from being damaged is not a particularly energy-intensive process, and so we have to look elsewhere for the reason why it hasn't been prioritized by evolution.

3. The Kitavan diet is high in digestible starch. The foods they eat have been characterized for starch content, glycemic index, and fiber content. Their diet overall has a high glycemic load, is 69% carbohydrate by calories, and is similar in calories to the American diet. They have a low BMI, a low fasting insulin and low fasting glucose. I agree that there are many factors at play here, and the example of the Kitavans doesn't necessarily give carbohydrate a free pass in all situations. But it does show that a high carbohydrate intake, at least under certain circumstances, is compatible with low fasting insulin, high insulin sensitivity, leanness, and apparent good health.

I also agree that the Kitavans are not really a good model of longevity. Although they live a long time relative to other non-industrial cultures, and have individuals exceeding 95 years old, they don't have a longer average lifespan than people in affluent nations. One can guess that it's due to a lack of modern medical care to treat infectious diseases, and I think that's likely to play a role, but ultimately it's speculation. It's an open question whether you could improve their lifespan by reducing the non-fiber carbohydrate content of their diet, but I'm skeptical.

In the end, it's also an open question whether or not you can extend life by restricting carbohydrate. For the typical overweight American who responds well to carbohydrate restriction, it's reasonable to speculate that it might. For an insulin-sensitive, lean American, it's not clear that it would have much benefit, outside of reducing potentially harmful foods such as gluten and sugar. Although insulin signaling is probably tied up with lifespan in humans, as in many other species, no one has shown that post-meal insulin spikes caused by carbohydrate, as opposed to chronically elevated insulin and insulin resistance, is harmful. The story is not as simple as "more serum insulin = shorter lifespan".

Is there any evidence that carbohydrate restriction extends lifespan in a non-carnivorous mammal such as a rodent or monkey? I'm open to the possibility, but I haven't seen any studies. I'll look forward to them.

Malocclusion: Disease of Civilization, Part IX

A Summary

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

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

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

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

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

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


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

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

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

Malocclusion: Disease of Civilization, Part VII

Jaw Development During Adolescence

Beginning at about age 11, the skull undergoes a growth spurt. This corresponds roughly with the growth spurt in the rest of the body, with the precise timing depending on gender and other factors. Growth continues until about age 17, when the last skull sutures cease growing and slowly fuse. One of these sutures runs along the center of the maxillary arch (the arch in the upper jaw), and contributes to the widening of the upper arch*:

This growth process involves MGP and osteocalcin, both vitamin K-dependent proteins. At the end of adolescence, the jaws have reached their final size and shape, and should be large enough to accommodate all teeth without crowding. This includes the third molars, or wisdom teeth, which will erupt shortly after this period.

Reduced Food Toughness Correlates with Malocclusion in Humans

When Dr. Robert Corruccini published his seminal paper in 1984 documenting rapid changes in occlusion in cultures around the world adopting modern foodways and lifestyles (see this post), he presented the theory that occlusion is influenced by chewing stress. In other words, the jaws require good exercise on a regular basis during growth to develop normal-sized bones and muscles. Although Dr. Corruccini wasn't the first to come up with the idea, he has probably done more than anyone else to advance it over the years.

Dr. Corruccini's paper is based on years of research in transitioning cultures, much of which he conducted personally. In 1981, he published a study of a rural Kentucky community in the process of adopting the modern diet and lifestyle. Their traditional diet was predominantly dried pork, cornbread fried in lard, game meat and home-grown fruit, vegetables and nuts. The older generation, raised on traditional foods, had much better occlusion than the younger generation, which had transitioned to softer and less nutritious modern foods. Dr. Corruccini found that food toughness correlated with proper occlusion in this population.

In another study published in 1985, Dr. Corruccini studied rural and urban Bengali youths. After collecting a variety of diet and socioeconomic information, he found that food toughness was the single best predictor of occlusion. Individuals who ate the toughest food had the best teeth. The second strongest association was a history of thumb sucking, which was associated with a higher prevalence of malocclusion**. Interestingly, twice as many urban youths had a history of thumb sucking as rural youths.

Not only do hunter-gatherers eat tough foods on a regular basis, they also often use their jaws as tools. For example, the anthropologist and arctic explorer Vilhjalmur Stefansson described how the Inuit chewed their leather boots and jackets nearly every day to soften them or prepare them for sewing. This is reflected in the extreme tooth wear of traditional Inuit and other hunter-gatherers.

Soft Food Causes Malocclusion in Animals

Now we have a bunch of associations that may or may not represent a cause-effect relationship. However, Dr. Corruccini and others have shown in a variety of animal models that soft food can produce malocclusion, independent of nutrition.

The first study was conducted in 1951. Investigators fed rats typical dry chow pellets, or the same pellets that had been crushed and softened in water. Rats fed the softened food during growth developed narrow arches and small mandibles (lower jaws) relative to rats fed dry pellets.

Other research groups have since repeated the findings in rodents, pigs and several species of primates (squirrel monkeys, baboons, and macaques). Animals typically developed narrow arches, a central aspect of malocclusion in modern humans. Some of the primates fed soft foods showed other malocclusions highly reminiscent of modern humans as well, such as crowded incisors and impacted third molars. These traits are exceptionally rare in wild primates.

One criticism of these studies is that they used extremely soft foods that are softer than the typical modern diet. This is how science works: you go for the extreme effects first. Then, if you see something, you refine your experiments. One of the most refined experiments I've seen so far was published by Dr. Daniel E. Leiberman of Harvard's anthropology department. They used the rock hyrax, an animal with a skull that bears some similarities to the human skull***.

Instead of feeding the animals hard food vs. mush, they fed them raw and dried food vs. cooked. This is closer to the situation in humans, where food is soft but still has some consistency. Hyrax fed cooked food showed a mild jaw underdevelopment reminiscent of modern humans. The underdeveloped areas were precisely those that received less strain during chewing.

Implications and Practical Considerations

Besides the direct implications for the developing jaws and face, I think this also suggests that physical stress may influence the development of other parts of the skeleton. Hunter-gatherers generally have thicker bones, larger joints, and more consistently well-developed shoulders and hips than modern humans. Physical stress is part of the human evolutionary template, and is probably critical for the normal development of the skeleton.

I think it's likely that food consistency influences occlusion in humans. In my opinion, it's a good idea to regularly include tough foods in a child's diet as soon as she is able to chew them properly and safely. This probably means waiting at least until the deciduous (baby) molars have erupted fully. Jerky, raw vegetables and fruit, tough cuts of meat, nuts, dry sausages, dried fruit, chicken bones and roasted corn are a few things that should stress the muscles and bones of the jaws and face enough to encourage normal development.


* These data represent many years of measurements collected by Dr. Arne Bjork, who used metallic implants in the maxilla to make precise measurements of arch growth over time in Danish youths. The graph is reproduced from the book A Synopsis of Craniofacial Growth, by Dr. Don M. Ranly. Data come from Dr. Bjork's findings published in the book Postnatal Growth and Development of the Maxillary Complex. You can see some of Dr. Bjork's data in the paper "Sutural Growth of the Upper Face Studied by the Implant Method" (free full text).

** I don't know if this was statistically significant at p less than 0.05. Dr. Corruccini uses a cutoff point of p less than 0.01 throughout the paper. He's a tough guy when it comes to statistics!

*** Retrognathic.

phil heath picture real or enhanced picture phil the gift heath looking massive full muscle bellies

now is this picture of phil heath real really shows phil heathand why he is seen as a potential mr olympia the muscle bellies on phil heath are phill hehe as in full.

not sure with this picture if it has been slightly tweaked or not to make phil look bigger, or if it is the angle that it is phographed at that gives that effect, but phil heath looks one of his most massive in the picture.

biecps on phil and triceps is one of the things phil heath is known for his arms must be getting close to 24 inches at times they look unreal.

also to balance out those massive biceps and triceps phil heath also has massive forearms in proportion with the upper arm muscles.

actually i think phil heath has had to train to bring up other body parts to balance out his arm size, like phil heath had to do a lot of should training to make up the balance between his arms.

Tips for Choosing the Correct Car Insurance Company

When you go to choose a car insurance company it may be a tough choice deciding which one is best. First, you have to decide what you are looking for in an auto insurance company
so that you can make the right decision. There are many insurance companies to choose from which can make your decision even more difficult. Here are a few things that can help you to choose the right insurance company for your needs.

You should definitely research several options before making your decision. This will be important as some of them will offer different packages and services. You should never let the cost be your deciding decision when it comes to choosing auto insurance. The price is an important factor but what is more important is the service you get for that price.

The price can vary quite a bit between the different companies due to some with offer services that some do not. By comparing insurance companies and what they have to offer you can help you to fill in the blanks as to what is included in the cost or not. If the company has good and reliable customer service this is another reason you may decide to choose a particular insurance company. The service you receive will be an important feature to look for with any car insurance company. Talk to them and compare their services to other companies. Make sure they are dependable so that you will be able to trust them with your auto insurance needs. Maybe a friend or family member can give you some advice on choosing a good auto insurance company. This is a good way to know if others have had good service with their insurance companies.

If you check online, each state should have a website about their states insurance companies. This is a good way to see how many complaints each insurance company has received from their customers. Online sites have so much information that they should definitely help you in making your decision much easier. Sometimes by going to a body shop around your town and asking them, they can give you good advice on which car insurance companies are the best. They deal with these companies on a daily basis so they should have information that will be helpful to you. Compare the companies to find out which of them have the best financial strength score. This is a good way to find out if the insurance company will have the means to pay for claims.
http://www.articlesbase.com/automotive-articles/tips-for-choosing-the-correct-car-insurance-company-1695047.html

Car Insurance Secrets, 8 Secrets Your Car Insurer Won't Tell You

Keeping your premiums from rising? That can feel like playing a game where the rule maker refuses to tell you the rules.

*If you have good credit, you'll pay less on car insurance.
Almost all car insurers including the top five pull your credit report.
Why? Studies have shown a direct correlation between your credit score and the likelihood that you will file a claim.
Car Insurers also know that if you pay your bills in a timely fashion and have had the same credit accounts for a long time, you're more stable than someone who pays late and frequently opens and closes accounts.
Car insurers use this information to create your "insurance risk score," which is one factor that determines your car insurance rate.

Tip: Your car insurance risk score is not available to you, but it may be similar to your credit score. If you have unusual credit activity, wait a month for it to return to normal before buying car insurance.

*Your car model affects your premium car insurance. You won't get these numbers from your Car insurer. But the car insurers do have a rating system for every car make and model.
Most use a system devised by the Car Insurance Services Office, which starts with the cost of the vehicle and then factors in safety and theft data.

Tip: You can file a claim on your home insurance. Most home insurance policies will cover smaller, less expensive items such as compact discs.

*Bad drivers will pay
You'll pay for your bad driving. The industry standard is to increase your premium by 40% of the insurer's base rate after your first at fault accident. Not all car insurers play by this rule.

Tip: Some car insurance companies have a forgive the first accident policy. So ask your Car insurance company if it has a forgiveness policy and how to qualify? .

*You'll pay for your friend's bad driving, too. If your friend borrows your car and crashes it, you'll have to file a claim with your car insurance company.

Tip: If your friend didn't have permission to take your car, in most cases you won't be held liable for the damage. But if your friend is uninsured and causes damage that exceeds your policy limits, the injured party can come after you for medical and property damage expenses.

*Your car's real worth
each car insurance company has its own proprietary list of car values.
The car insurance company may also ask local dealers what they'd charge for a similar replacement car.

Tip: If you disagree with your car insurance company's value determination, there are several things you can do:
Next time, get gap insurance. It wil l pay the difference between what an car insurer will cover and what you owe.
If you have maintenance records that show you've had the oil changed every 3,000 miles and you've had the car checked routinely by a mechanic.
If you've been paying premiums on any special parts or upgrades, make sure those are included in the car insurance company's evaluation.

*Odds and ends
Hit by an uninsured motorist? Try to "stack." (UM/UIM) coverages means collecting from more than one car insurance policy that you hold.

Tip: Check the language of your car insurance policy to see if stacking is allowed.
There are two scenarios for stacking:
First, if you have multiple cars on your car insurance policy with UM/UIM coverage on each, you can collect the limit of your UM/UIM coverage under as many vehicles as necessary to cover full payment for damages.
Second, if you have more than one car insurance policy with UM/UIM coverage, even if they're from two different car insurers, you can make a claim under each policy until all your damages are recovered.

*You can wait to add your teenager to your car insurance policy until he or she is licensed.

Tip: Don't forget to tell your car insurance company that you have a licensed teen. If you have to file a claim on his or her behalf, your car insurance company is entitled to charge you back premiums from the date your teen received a license.

*You must officially cancel your car insurance policy when you switch car insurers. you can cancel your car insurance coverage at any time by notifying the car insurance company in writing of the date of termination.

Tip: Call your car insurance agent and let him know you are canceling your car insurance policy. Give a specific date, or you may end up uninsured for a period of time.
The car insurance company will send you a cancellation request. Most often, the form is already filled out and all it requires is your signature.