The Coronary Heart Disease Epidemic

Few people alive today are old enough to remember the beginning of the coronary heart disease (CHD) epidemic in the 1920s and 1930s, when physicians in the U.S. and U.K. began sounding alarm bells that an uncommon disease was rapidly becoming the leading cause of death. By the 1950s, their predictions had come true. A decade later, a new generation of physicians replaced their predecessors and began to doubt that heart attacks had ever been rare. Gradually, the idea that the disease was once uncommon faded from the public consciousness, and heart attacks were seen as an eternal plague of humankind, avoided only by dying of something else first.

According to U.S. National Vital Statistics records beginning in 1900, CHD was rarely given as the cause of death by physicians until after 1930. The following graph is from The Great Cholesterol Con, by Anthony Colpo, which I highly recommend.


The relevant line for CHD deaths begins in the lower left-hand part of the graph. Other types of heart disease, such as heart failure due to cardiomyopathy, were fairly common and well recognized at the time. These data are highly susceptible to bias because they depend on the physician's perception of the cause of death, and are not adjusted for the mean age of the population. In other words, if a diagnosis of CHD wasn't "popular" in 1920, its prevalence could have been underestimated. The invention of new technologies such as the electrocardiogram facilitated diagnosis. Changes in diagnostic criteria also affected the data; you can see them as discontinuities in 1948, 1968 and 1979. For these reasons, the trend above isn't a serious challenge to the idea that CHD has always been a common cause of death in humans who reach a certain age.

This idea was weakened in 1951 with the publication of a paper in the Lancet medical journal titled "Recent History of Coronary Disease", by Dr. Jerry N. Morris. Dr. Morris sifted through the autopsy records of London Hospital and recorded the frequency of coronary thrombosis (artery blockage in the heart) and myocardial infarction (MI; loss of oxygen to the heart muscle) over the period 1907-1949. MI is the technical term for a heart attack, and it can be caused by coronary thrombosis. Europe has a long history of autopsy study, and London Hospital had a long-standing policy of routine autopsies during which they kept detailed records of the state of the heart and coronary arteries. Here's what he found:

The dashed line is the relevant one. This is a massive increase in the prevalence of CHD death that cannot be explained by changes in average lifespan. Although the average lifespan increased considerably over that time period, most of the increase was due to reduced infant mortality. The graph only includes autopsies performed on people 35-70 years old. Life expectancy at age 35 changed by less than 10 years over the same time period. The other possible source of bias is in the diagnosis. Physicians may have been less likely to search for signs of MI when the diagnosis was not "popular". Morris addresses this in the paper:

The first possibility, of course, is that the increase is not real but merely reflects better post-mortem diagnosis. This is an unlikely explanation. There is abundant evidence throughout the forty years that the department was fully aware of the relation of infarction to thrombosis, of myocardial fibrosis to gradual occlusion, and of the topical pathology of ostial stenosis and infarction from embolism, as indeed were many pathologists last century... But what makes figures like these important is that, unlike other series of this kind, they are based on the routine examination at necropsy of the myocardium and of the coronary arteries over the whole period. Moreover Prof. H. M. Turnbull, director of the department, was making a special case of atheroma and arterial disease in general during 1907-1914 (Turnbull 1915). The possibility that cases were overlooked is therefore small, and the earlier material is as likely to be reliable as the later.

Dr. Morris's study was followed by another similar one published in 1985 in the journal Medical History, titled "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982", conducted by Dr. Robert Finlayson. This study, in my opinion, is the coup de grace. Finlayson systematically scrutinized autopsy reports from St. Bartholemew's hospital, which had conducted routine and detailed cardiac autopsies since 1868, and applied modern diagnostic criteria to the records. He also compared the records from St. Bartholemew's to those from the city mortuary. Here's what he found:

The solid line is MI mortality. Striking, isn't it? The other lines are tobacco and cigarette consumption. These data are not age-adjusted, but if you look at the raw data tables provided in the paper, some of which are grouped by age, it's clear that average lifespan doesn't explain much of the change. Heart attacks are largely an occurrence of the last 80 years, and were almost totally unknown before the turn of the 20th century.

What caused the epidemic? Both Drs. Morris and Finlayson also collected data on the prevalence of atherosclerosis (plaques in the arteries) over the same time period. Dr. Morris concluded that the prevalence of severe atherosclerosis had decreased by about 50% (although mild atherosclerosis such as fatty streaks had increased), while Dr. Finlayson found that it had remained approximately the same:


He found the same trend in females. This casts doubt on the idea that coronary atherosclerosis is sufficient in and of itself to cause heart attacks, although modern studies have found a strong association between advanced atherosclerosis and the risk of heart attack on an individual level. Heart attacks are caused by several factors, one of which is atherosclerosis.  Atherosclerosis can be caused by infectious disease, so this may explain Dr. Morris's finding that it has decreased since the beginning of the 20th century.

What changes in diet and lifestyle associated with the explosion of MI in the U.K. and U.S. after 1920? Dr. Finlayson has given us a hint in the graph above: cigarette consumption increased dramatically over the same time period, and closely paralleled MI mortality. Smoking cigarettes is very strongly associated with heart attacks in observational studies. Animal studies also support the theory. While I believe cigarettes are an aggravating factor, I do not believe they are the main cause of the MI epidemic. Dr. Finlayson touched on a few other factors in the text of the paper, and of course I have my own two cents to add. I'll discuss that next time.

Menyuburkan Rambut Dengan Telur Udang

Bahan-Bahan :Udang besar yang mengandung telur ............. 3 ekorCara Pembuatan :Ambillah telur udang tersebut dan letakan dalam sebuah wadah.Aturan Pakai :Gosok-gosokkan telur udang tadi pada bagian yang botak atau pada bagian yang kurang subur tumbuh rambutnya pada sore. Lakukan hal tersebut sebelum menjelang tidur. Biarkan demikian selama satu malam. Pada pagi harinya, cucilah bersamaan

Dihydro-Vitamin K1

Step right up ladies and gents; I have a new miracle vitamin for you. Totally unknown to our ignorant pre-industrial ancestors, it's called dihydro-vitamin K1. It's formed during the oil hydrogenation process, so the richest sources are hydrogenated fats like margarine, shortening and commercial deep fry oil. Some of its benefits may include:

• Inhibiting vitamin K2 metabolism
• Reducing bone mineral density
  
• Causing organ damage and inhibiting platelet formation in animal models
• Dramatically increasing the death rate of spontaneously hypertensive rats

Dihydro-vitamin K1 accounts for roughly 30% of the vitamin K intake of American children, and a substantial portion of adult intake as well. Over 99 percent of Americans have it in their diet. Research on dihydro-vitamin K1 is in its infancy at this point, so no one has a very solid idea of its effects on the body beyond some preliminary and disturbing suggestions from animal experiments and brief human trials.

This could be another mechanism by which industrially processed vegetable oils degrade health. It's also another example of why it's not a good idea to chemically alter food. We don't understand food, or our bodies, well enough to know the long-term consequences of foods that have been recently introduced to the human diet. I believe these foods should be avoided on principle.

Pastured Eggs

Eggs are an exceptionally nutritious food. It's not surprising, considering they contain everything necessary to build a chick! But all eggs are not created equal. Anyone who has seen the tall, orange yolk, viscous white, and tough shell of a true pastured egg knows they're profoundly different. So has anyone who's tasted one. This has been vigorously denied by the American Egg Board and the Egg Nutrition Council, primarily representing conventional egg farmers, which assert that eggs from giant smelly barns are nutritionally equal to their pastured counterparts.

In 2007, the magazine Mother Earth News decided to test that claim. They sent for pastured eggs from 14 farms around the U.S., tested them for a number of nutrients, and compared them to the figures listed in the USDA Nutrient Database for conventional eggs. Here are the results per 100 grams for conventional eggs, the average of all the pastured eggs, and eggs from Skagit River Ranch, which sells at my farmer's market:

Vitamin A:

• Conventional: 487 IU
• Pastured avg: 792 IU
• Skagit Ranch: 1013 IU
  

Vitamin D:

• Conventional: 34 IU
  
• Pastured avg: 136 - 204 IU
  
• Skagit Ranch: not determined
  

Vitamin E:

• Conventional: 0.97 mg
• Pastured avg: 3.73 mg
  
• Skagit Ranch: 4.02 mg

Beta-carotene:

• Conventional: 10 mcg
  
• Pastured avg: 79 mcg
  
• Skagit Ranch: 100 mcg
  

Omega-3 fatty acids:

• Conventional: 0.22 g
  
• Pastured avg: 0.66 g
  
• Skagit Ranch: 0.74 g
  

Looks like the American Egg Board and the Egg Nutrition Council have some egg on their faces...

Eggs also contain vitamin K2, with the amount varying substantially according to the hen's diet. Guess where the A, D, K2, beta-carotene and omega-3 fatty acids are? In the yolk of course. Throwing the yolk away turns this powerhouse into a bland, nutritionally unimpressive food.

It's important to note that "free range" supermarket eggs are nutritionally similar to conventional eggs. The reason pastured eggs are so nutritious is that the chickens get to supplement their diets with abundant fresh plants and insects. Having little doors on the side of a giant smelly barn just doesn't replicate that.

Vitamin A, Vitamin D and Osteoporosis Reprise

Chris Masterjohn just pointed out a new study that examined the relationship of vitamin A to osteoporosis in the context of vitamin D intake. The study is part of the massive Women's Health Initiative, which involved over 75,000 women. The conclusion:

No association between vitamin A or retinol intake and the risk of hip or total fractures was observed in postmenopausal women. Only a modest increase in total fracture risk with high vitamin A and retinol intakes was observed in the low vitamin D-intake group.

In other words, only women with a low vitamin D intake (less than 440 IU per day) had an increased likelihood of fracture at high vitamin A intakes (more than 8,000 IU per day). This is consistent with the hypothesis that an above-average intake of vitamin A only increases the risk of osteoporosis in the presence of low vitamin D, and that vitamin D deficiency, not vitamin A excess, is the true problem. Hop over to Chris's post for more details.

Vitamin A on Trial: Does Vitamin A Cause Osteoporosis?
Is Vitamin A Toxicity a Concern?

Iodine

I recently saw a post on Dr. Davis's Heart Scan Blog that reminded me I intended to write about iodine. Iodine is an essential trace mineral. It's required for the formation of activated thyroid hormones T3 and T4. The amount of thyroid hormones in circulation, and the body's sensitivity to them, strongly influences metabolic rate. Iodine deficiency can lead to weight gain and low energy. In more severe cases, it can produce goiter, an enlargement of the thyroid gland.

Iodine deficiency is also the most common cause of preventable mental retardation worldwide. Iodine is required for the development of the nervous system, and also concentrates in a number of other tissues including the eyes, the salivary glands and the mammary glands.

There's a trend in the alternative health community to use unrefined sea salt rather than refined iodized salt. Personally, I use unrefined sea salt on principle, although I'm not convinced refined iodized salt is a problem. But the switch removes the main source of iodine in most peoples' diets, creating the potential for deficiency in some areas. Most notably, the soil in the midwestern United States is poor in iodine and deficiency was common before the introduction of iodized salt.

The natural solution? Sea vegetables. They're rich in iodine, other trace minerals, and flavor. I like to add a 2-inch strip of kombu to my beans. Kombu is a type of kelp. It adds minerals, and is commonly thought to speed the cooking and improve the digestion of beans and grains.

Dulse is a type of sea vegetable that's traditionally North American. It has a salty, savory flavor and a delicate texture. It's great in soups or by itself as a snack.

And then there's wakame, which is delicious in miso soup. Iodine is volatile so freshness matters. Store sea vegetables in a sealed container. It may be possible to overdo iodine, so it's best to eat sea vegetables regularly but in moderation like the Japanese.

Seafood such as fish and shellfish are rich in iodine, especially if fish heads are used to make soup stock. Dairy is a decent source in areas that have sufficient iodine in the soil.

Cod liver oil is another good source of iodine, or at least it was before the advent of modern refining techniques. I don't know if refined cod liver oil contains iodine. I suspect that fermented cod liver oil is still a good source of iodine because it isn't refined.

Omega-6 Linoleic Acid Suppresses Thyroid Signaling

Excess Omega-6 Fat Damages Infants' Livers

A nurse friend of mine sent me an e-mail a few weeks ago with a very interesting observation:

On the unit I work on we get lots of babies who have "short gut syndrome" due to a variety of causes who have to be on parenteral nutrition to supplement their nutrition while their GI system grows and hopefully heals fast enough. The big problem (among many) with TPN (total parenteral nutrition) is that it destroys the liver and kids get horribly jaundiced (which also causes brain damage) and often they die of liver failure or need a liver transplant before their GI system grows enough to take them off TPN.

Boston Children's has done some amazing work showing that this is largely due to the fact that the lipids part of the TPN was a soybean based oil so they started using Omegaven instead which is a fish oil based IV lipid solution. So far the results have been amazing and reversed the damage in lots of kids livers and prevented it in those started on Omegaven at birth.

Babies born with short gut syndrome can't absorb nutrients properly due to their unusually short small intestine. They're temporarily fed intravenously (total parenteral nutrition; TPN), until their intestines can develop enough to digest food normally.

The typical TPN formula contains soybean and safflower oils as the fat, both of which are over 50% omega-6 linoleic acid. Soybean oil also contains 7% omega-3 alpha-linolenic acid. You can't get the kids started too early on a "heart-healthy" diet!

The solution was to replace the vegetable oil with fish oil, which prevents or rapidly reverses the severe liver damage caused by TPN rich in omega-6 vegetable oils. I don't think this is a great solution, but it certainly beats vegetable oil. The ideal solution would be to replace the vegetable oil with a fat that approximates the composition of breast milk: mostly monounsaturated and saturated fat, with a little bit of linoleic acid, alpha-linolenic acid and long-chain fats such as AA and DHA. You could do this pretty easily with a mix of lard and fish oil; or palm oil and fish oil; or coconut oil, olive oil and fish oil. Breast milk composition varies with diet, and the amount of linoleic acid in the breast milk of Western populations is unusually high.

Excess linoleic acid, particularly when combined with excess fructose and insufficient omega-3 fat, is toxic to the liver. Modern Western nations are experiencing an epidemic of non-alcoholic fatty liver disease (NAFLD), which animal studies indicate is probably the result of replacing animal fats with polyunsaturated vegetable oils and increasing sugar intake (see links below for more detail). Fatty liver was seen primarily in alcoholics three decades ago. An estimated 1/4 of Americans now have NAFLD. It's the number one cause of liver damage in the U.S.

Where the liver goes, the rest of the body follows.

How to Fatten Your Liver
Nonalcoholic Fatty Liver Disease
The Liver: Your Metabolic Gatekeeper
More Liver Functions