The Flower Cottages

Since it's so hot outside, I decided to paint a little in some air conditioning. I will write more about Sedona in my next blog, but here is the painting I did and the picture I created it from. I took the picture in Provincetown, MA last June when I was visiting. These cottages are right on the water right before you get to town. They are beautiful. Click HERE for more information about these historic cottages. I love them.

Disclaimer: Do not go on the beach to take photos. It is NOT allowed. You will be trespassing and asked to leave or fined. I have no idea how I got on the beach to take the shot.

Mile 0...The Beginning

I have a few goals for myself on this trip and one of them is to paint. Try to paint, rather. I took this picture of Mile 0 (see actual picture on the "On Your Mark..." blog) in Utah last summer on my journey with Maggie. I am looking forward to taking more pictures and writing a bit while I am on the road. At this moment, I am driving. I will keep you posted on where I go and what I am doing. I have a feeling that I will soon be surrounded by some magnificent sights coming up. I'm sure at this point, I am driving through the heat, starting a conversation with my inner voice. I know Max will not keep me company since he seems to find anything to lay on but the two beds I put out for him in the car. Until the next stop...

The Diet-Heart Hypothesis: Subdividing Lipoproteins

Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk.

Lipoproteins Can be Subdivided into Several Subcategories

In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):

The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease.

Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder.

Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).

Diet Affects LDL Subcategories

The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):

Out of the 87 men with pattern A on the high-fat diet, 36 converted to pattern B on the low-fat diet... Taken together, these results indicate that in the majority of men, the reduction in LDL cholesterol seen on a low-fat, high-carbohydrate diet is mainly because of a shift from larger, more cholesterol-enriched LDL to smaller, cholesterol-depleted LDL [sdLDL].

In other words, in the majority of people, high-carbohydrate diets lower LDL cholesterol not by decreasing LDL particle count (which might be good), but by decreasing LDL size and increasing sdLDL (probably not good). This has been shown repeatedly, including with a 10% fat diet and in children. However, in people who already exhibit pattern B, reducing fat does reduce LDL particle number. Keep in mind that the majority of carbohydrate in modern America comes from refined wheat and sugar; a diet of unrefined carbohydrate may not have these effects.

Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:

In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid [as well as palmitic acid], was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate [density] were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL.

Participants who ate the most saturated fat had the largest LDL, and vice versa. Kudos to Dr. Krauss for publishing these provocative data. It's not an isolated finding. He noted in 1994 that:

Cross-sectional population analyses have suggested an association between reduced LDL particle size and relatively reduced dietary animal-fat intake, and increased consumption of carbohydrates.

Diet Affects HDL Subcategories

Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:

The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.

Saturated and omega-3 fats selectively increase large HDL. Dr. B. G. of Animal Pharm has written about this a number of times.

Wrapping it Up

Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are refined wheat and sugar.  Healthier sources of carbohydrate have different effects on blood lipids.
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.

On Your Mark...

The beginning. With the start of anything new, emotions can be filled with excitement, nervousness, fear or hope.

This trip is a mix bag of all.

Someone very special to me told me to write what I have done and not what I plan to do so, perhaps I am breaking the rules on this one.

I am leaving Southern California tomorrow to head out on the road. House is rented, car is packed and the adventure is about to begin.

I learned a few things from my last trip so here are some tips if you are headed out on a summer road trip (not in any particular order):

-Have something prepared to listen to (music, inner voices, etc.)

- Don't play the gas game (sometimes I like to stress myself out by seeing how far I can get on the fumes left in the tank when I am in the middle of nowhere)

- Remember that the navigator is your friend (mine is named Cindy and we have a love/hate relationship sometimes)

- Camp books come in handy

- Keep cash in the car for the East Coast (Toll Roads)

- Be Flexible in your plans (you never know when you will ever get to see the largest ball of twine again)

- I like to think that animals are just sleeping on the side of the road

- It's not a good idea to give dog treats to raccoons, unless you want the entire family over

- If you want Amish people to run away and hide from you, put a bathing suit on

- In Oregon, there is no self service gas pump. Not a good idea to argue who is going to pump gas

- There are certain states where it’s cheaper to injure or kill a road worker than others.

- Purell is your friend

and lastly...

- Don't camp next to a retired man camping with his cat while blowing into a harmonica in Utah (Trust me on this one).

What have you learned about road travel that you want to pass along?

Inside Out Rings

What's in a ring?

If you are wearing one of Holly Riddel's creations, you would have a semi-precious stone touching your skin. It's not your everyday ring. In fact, the concept of the ring is for making a commitment to yourself. Why not be the change in your own life?

I heard about these rings over a year ago and besides being beautiful, they fascinated me. What a perfect way to make a commitment to yourself and have it on your finger as a daily reminder of that commitment. I was sold. I put my order in and waited patiently for the ring to arrive. Once it came, I couldn't wait to put it on and not take it off. That is exactly what I did.

With this ring on my finger, I headed out on the open road with my dog, Maggie and our 4x9 teardrop trailer. A commitment to be true to myself and embark on a journey of a lifetime. Everyday I would look at my ring and feel it with my thumb by habit.

I was in Michigan at a truck stop when I went in to quickly use the restroom after filling up at the gas station. Moments later when my thumb brushed up against my finger to feel the ring, it was gone. A rush of panic filled through my body instantly. I felt sick. I went back to the truck stop and went through the trash can picking out every paper towel and other "trash" items. No ring. It slipped off of my finger as I was washing my hands and I will never get it back. I was crushed.

It's amazing how a ring could bring up so much emotion. I now have a replacement for the one that was lost. I received it today for this new journey and commitment I have made to myself.

Thank you Holly for being an inspiration and making a difference in peoples lives. For more information on Holly and her inside out rings, click here.

MRFIT Mortality

The Multiple Risk Factor Intervention trial was a very large controlled diet trial conducted in the 1980s. It involved an initial phase in which investigators screened over 350,000 men age 35-57 for cardiovascular risk factors including total blood cholesterol. 12,866 participants with major cardiovascular risk factors were selected for the diet intervention trial, while the rest were followed for six years. I discussed the intervention trial here.

During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):


Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.

Possible explanations from other studies include higher infection rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.

The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.

2 Days

As I write this, I am realizing that I only have 2 more full days of being in my home. I have renters coming to live here while I travel the country. The past few weeks I've been going through all of my things to get the house ready for their stay. I knew it was going to be a lot of work, however I never expected it to be so emotional.

I've lived in this home for 7 years, so I haven't been through my things in a long time. Every drawer, cabinet, closet and hiding place was uncovered. It's been a cleansing of the soul, in a way. Mostly, it was a realization that I have too much crap.

I am going to be living out of a car for the next few months and I can guarantee that I will not miss any of my "treasures" left behind. I know I will miss my bed and a hot shower right next to each other, but as far as items go, there is nothing I will think about.

In fact, I could get rid of more things. I donated most of my clothes since I swim in them now, sold a few things on Craig's list, and recycled items I no longer needed. It's safe to say that once I return...not much is coming back into the house.

For me, road trips are a great way to clear the mind. As I mentioned in my blogs before, it can be therapeutic. There is so much to see in this country, I am excited to see some new and amazing places.

The road is my blank canvas. I will paint the journey with every mile driven. Just me and my co-pilot, Max. We look forward to sharing our moments with you here.

The Diet-Heart Hypothesis: A Little Perspective

Now that we've discussed the first half of the diet-heart hypothesis, that saturated fat elevated total and LDL cholesterol, let's take a look at the second half. This is the idea that elevated serum cholesterol causes cardiovascular disease, also called the "lipid hypothesis".

Heart Attack Mortality vs. Total Mortality

We've been warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups: If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group.

Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.): Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population.

These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.

The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). This suggests that total blood cholesterol as a marker of heart attack risk is not universal. It would not necessarily apply to someone eating a non-Western diet.

Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value

So far, this probably hasn't shocked anyone. Most people agree that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets (lipoproteins) containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.

The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.

The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is substantially higher than someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this observation in a future post.

In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins).

Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is some combination of high LDL (particularly LDL particle number), low HDL, and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.

The Diet-Heart Hypothesis: Stuck at the Starting Gate?

The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack.

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because the evidence that typical dietary amounts cause heart disease in humans is weak.  Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the main source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 eggs per week (click for larger image): The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not have a large impact on serum cholesterol in the long term, perhaps because humans are adapted to eating cholesterol. Most people are able to adjust their own cholesterol metabolism to compensate when the amount in the diet increases. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology.

The first half of the diet-heart hypothesis states that eating saturated fat raises blood cholesterol. This has been accepted without much challenge by diet-health authorities for nearly half a century. In 1957, Dr. Ancel Keys proposed a formula (Lancet 2:1959. 1957) to predict changes in total cholesterol based on the amount of saturated and polyunsaturated fat in the diet. This formula, based primarily on short-term trials from the 1950s, stated that saturated fat is the primary dietary influence on blood cholesterol.

According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were significant flaws in the data from the very beginning, which were pointed out in this critical 1973 literature review in the American Journal of Clinical Nutrition (free full text).

The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect sometimes had more to do with LA lowering blood cholesterol than saturated fat raising it. This is not at all what I was expecting to find when I began looking through these trials.

Reading through the short-term controlled trials, I was surprised by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and non-optimal study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and consistently demonstrable.  

The long-term data are not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA certainly does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).  The small changes that did occur could have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions.

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Disease by Dr. Harumi Okuyama et al.): What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). 

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not the case. The Masai traditionally get a high proportion of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating practically nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man? Junk food.

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s).  Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Does dietary saturated fat influence total cholesterol and LDL over the long term?  I don't have the answers, but I do think it's interesting that the evidence is much less consistent than it's made out to be.  It may be that if dietary saturated fat influences total cholesterol or LDL concentration in the long term, the effect is is secondary to other factors.  That being said, it's clear that linoleic acid, in large amount, reduces circulating total cholesterol and LDL.

Dog Park

My attempt at getting some action pictures of Max at the dog park. I am fortunate that he gets along with most all dogs, even large ones! Even thought the tennis ball is about the size of his head, he still enjoys fetching it. He's been a good dog, still getting used to his name. I am the lucky one.

American Life Today

Wouldn't it be nice to meet an American, everyday?

As I traveled on my road trip last year, I expected to see some amazing places. I didn't expect to meet some of the most fascinating people along the way.

As I listened to their stories, I thought that there needs to be a way where people could learn about their life! Who is going to tell their story? How about them! I found it exhilarating to listen to personal stories from all walks of life in campgrounds, restaurants, parks, and truck stops.

That's how American Life Today.com came about. I wanted to capture the "everyday" American life asking them 5 questions, to keep it simple. Because you know how it is when granddad dips into the "juice" at the campsite...he can go on and on. I wanted to share just enough to keep you interested and awake, as well as promote a favorite charity.

Some of your stories have moved me to tears.

As sad as it is, the site will come to a close soon. I am going to start another journey in the next few weeks so I will schedule all of the remaining profiles that are waiting to post. After that, I will post as they come in but I will no longer beg you to answer the questions. You know I did!

A big THANK YOU to those of you who took the time to share your life. I know that people have enjoyed reading them, especially me.

Until the next adventure...

The Finnish Mental Hospital Trial

This diet trial was conducted between 1959 and 1971 in two psychiatric hospitals near Helsinki, Finland. One hospital served typical fare, including full-fat milk and butter, while the other served "filled milk", margarine and polyunsaturated vegetable oils. Filled milk has had its fat removed and replaced by an emulsion of vegetable oil. As a result, the diet of the patients in the latter hospital was low in saturated fat and cholesterol, and high in polyunsaturated fat compared to the former hospital. At the end of six years, the hospitals switched diets. This is known as a "crossover" design.

The results were originally published in 1972 in the Lancet (ref), and a subset of the data were re-published in 1979 in the International Journal of Epidemiology (ref). They found that during the periods that patients were eating the diet low in saturated fat and cholesterol, and high in vegetable oil, male participants (but not females) had roughly half the incidence of heart attack deaths. There were no significant differences in total mortality in either men or women. The female data were omitted in the 1979 report.

This study is often cited as support for the idea that saturated fat increases the risk of heart attack. The reason it's cited so often is it's one of a minority of trials that came to that conclusion. The only other controlled trial I'm aware of that replaced animal fat with polyunsaturated vegetable oil (without changing other variables at the same time) and found a statistically significant decrease in cardiovascular deaths was the Los Angeles Veterans' Administration study. However, there was no difference in total mortality, and there were significantly more heavy smokers in the control group. The difference in heart attack deaths in the V.A. trial was 18%, far less than the difference seen in the Finnish trial.

I can cite three controlled trials that came to the opposite conclusion, that switching saturated fat for vegetable oil increases cardiovascular mortality and/or total mortality: the Anti-Coronary Club Trial (4 years), the Rose et al. corn oil trial (2 years), and the Sydney Diet-Heart trial (5 years). Other controlled trials found no difference in total mortality or heart attack mortality from this intervention, including the National Diet-Heart Study (2 years) and the Medical Research Council study (7 years). Thus, the Finnish trial is an outlier whose findings have never been replicated by better-conducted trials.

I have three main bones to pick with the Finnish trial. The first two are pretty bad, but the third is simply fatal to its use as support for the idea that saturated fat contributes to cardiovascular risk:

1) A "crossover" study design is not an appropriate way to study a disease with a long incubation period. How do you know that the heart attacks you're observing came from the present diet and not the one the patients were eating for the six years before that? The Finnish trial was the only trial of its nature ever to use a crossover design.

2) The study wasn't blinded. When one wants to eliminate bias in diagnosis for these types of studies, one designs the study so that the physician doesn't know which group the patients came from. That way he can't influence the results, consciously or unconsciously. Obviously there was no way to blind the physicians in this study, because they knew what the patients in each hospital were eating. I think it's interesting that the only outcome not susceptible to diagnostic bias, total mortality, showed no significant changes in either men or women.

3) The Finnish Mental Hospital trial was not actually a controlled trial. In an editorial in the November 1972 issue of the Lancet, Drs. John Rivers and John Yudkin pointed out, among other things, that the amount of sugar varied by almost 50% between diet periods. In the December 30th issue, the lead author of the study responded:

In view of the design of the experiment the variations in sugar intake were, of course, regrettable. They were due to the fact that, aside from the fatty-acid composition and the cholesterol content of the diets, the hospitals, for practical reasons, had to be granted certain freedom in dietary matters.

In other words, the diets of the two hospitals differed significantly in ways other than their fat composition. Sugar was one difference. Carbohydrate intake varied by as much as 17% and total fat intake by as much as 26% between diet periods (on average, carbohydrate was lower and total fat was higher in the polyunsaturated fat group). The use of psychiatric drugs with known cardiovascular side effects differed substantially between groups and could have accounted for some of the difference in cardiovascular events.  

The definition of a controlled trial is an experiment in which all variables are kept reasonably constant except the one being evaluated. Therefore, the Finnish trial cannot rightfully be called a controlled trial. The fact that the result has never been replicated casts further doubt on the study.
I could continue listing other problems with the study, such as the fact that the hospital population included in the analysis had a high turnover rate (variable, but as high as 40%), and patients were included in the analysis even if they were at the hospital for as little as 50% of the time between first admission and final discharge (i.e., they came and went). But what's the use in beating a dead horse?

Planning his Escape

It's been a while since I've painted so I decided to give it a shot. Here is Max in the gate which should be called "Heeeeeere's MAX." He's a bit of a devil I am finding. I know this is nothing like what Kellie Straw does with her dogs, but it sorta looks like Max so that is success to me.

Travels with Max

I am about to begin another cross country road trip. The past few weeks I’ve been preparing to leave and this time, I am renting my home. I am lucky enough to be able to have a nice young couple and their chocolate lab stay here while Max and I embark on our adventure.

This time, it’s going to be different.

“Trailie” is staying home, Max and I are going to camp with a tent, I am going to read more, journal more and paint a little. I have a general timeline but I don’t know what path we will take yet. I have two weeks to decide which roads we will embark on, or perhaps we will leave and decide as we go.

Renting out your home is a journey in itself. I’ve lived here for 7 years and when you settle in a place, you usually don’t take the time to see what you have. I am going through and cleaning all cupboards, drawers, closets…everything. It’s a lot of “stuff.” Doing this cleanses the soul in a way. I am not attached to things as I once was. As time consuming and exhausting as it is, it brings a sense of relief to find homes for unwanted items and to purge the things I haven’t looked at or missed in years.

Max is settling in just fine. He is now guarding the house and is used to our little routine we have around here. It’s nice. We are bonding. I introduced him to “trailie” the other day and told him about the adventure Maggie and I had last summer. I broke down and cried. He slept at my feet.

Max and I will document our journey here so you can see what we are up to. I would love to hear of a destination that holds a special place with you.

Max

I can't imagine my life without a pet. I've had cats, dogs, guinea pigs, turtles, and fish as pets growing up. As you know from my travels, Maggie and I had the trip of a lifetime last summer. The past few months have been incredibly hard not having her around. She was with me for 10 years. Moved with me 4 times. Visited 26 States together.

Last Sunday, I went to the Farmer's market to pick up some strawberries and came home with a new family member. His name is Max. His time was up at a local shelter and a rescue group saved him on his last day. I took him out of the group cage to spend some time together and he didn't leave my side. I didn't want him to. I was instantly smitten.

I haven't had a small dog in the house for 23 years. My last 2 dogs were both larger so it's an adjustment. For instance, you need to bend lower to the ground to pet them, watch where you step so you don't crush them, buy smaller toys, less food, softer play and it's harder to hide your "does my butt look big in these jeans?" days with a smaller dog in a picture. Now there is nowhere to hide. Your butt looks even bigger. Not that you turn around and squat with pictures with your dog. Never mind. Anyway...

No, I am not going to carry him in a purse.

One of the things we are enjoying is going to the dog park and the dog beach. This was something I could never enjoy with Maggie since she would try to attack anything that wasn't a human. A bit of a buzz kill.

I look forward to this new chapter. I am excited about taking Max on new adventures. I think another trip is in order. Soon.

Here are some pictures from his week of making friends at the park and playing at the beach: