Well it’s been 2 weeks since Dave issued the Challenge and I’m stuck. I had a few to many cheat meals and a few to many cocktails. Dave is down 6 pounds following a grueling training schedule in his preparation for the Chicago Marathon.

He asked me not to share it as it was created specifically for him by his trainer but I can say that it would leave most of us half alive after the first 2 days. Kudos to Dave for enduring.

Time for me to kick it into high gear. Dave is basically doing two-a-days until race day October 10th. I went to the gym Monday night and then went cocktailing last night.

In Good Calories, Bad Calories Gary Taubes reviews the medical research that established connections between fat and cholesterol in our diets and heart disease. Traubs shows how this well accepted dogma has never been proven and makes a clear case that carbohydrates are responsible for obesity. The “diseases of civilization” are exacerbated by following the advice of these studies and subscribing to a fat is bad hypothesis.

I’m currently reading the first section and the reviews of the research that lead us to believe in low-fat diets is startling.

Here are a few truths that most Americans, including doctors, would consider blasphemous.

• Dietary fat does not make us fat
• The link to dietary cholesterol and blood cholesterol levels is very weak or non-existant
• Lowering total cholesterol does not improve mortality rates

Wild and crazy I know. Read the book…it will make more sense.

Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Vintage)
Price: 11.53

64 used & new available from 8.47

For decades we have been taught that fat is bad for us, carbohydrates better, and that the key to a healthy weight is eating less and exercising more. Yet despite this advice, we have seen unprecedented epidemics of obesity and diabetes. Taubes argues that the problem lies in refined carbohydrates, like white flour, easily digested starches, and sugars, and that the key to good health is the kind of calories we take in, not the number. In this groundbreaking book, award-winning science writer Gary Taubes shows us that almost everything we believe about the nature of a healthy diet is wrong.

Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health (Vintage)
Price: 11.53

64 used & new available from 8.47

The trusty Garmin was fully charged for today’s ride.

I stopped by the pool to meet Laura for a bit. I somehow resisted the urge to jump in. I don’t understand how the tri guys can jump on a bike with soaking wet shorts.

After stopping by the pool I headed down Wydown to the Starbucks and had some tea. On the way back I caught up to the SLU cycling team (stuck at a stop light) and got dropped pretty quickly.

I swung by Laura’s house and we rode over to the Festival of Nations at Tower Grove Park. We didn’t feel like we’d had enough festivities so we cruised over to LouFest at Forest Park. Unfortunately, it was $35 to get in so we had a cocktail at The Boathouse instead.

I rode with Laura back to her house and the Garmin started to complain about its battery so I cranked home pretty fast. I rode 27.7 miles in all and the last 3 where at about 15mph. A pretty good day. Taking a few breaks for tea, kabobs and the like is kind of nice. I imagine if I were super motivated I could ride 30 miles non-stop but why suffer when I’m just out for a good time.

It’s interesting how motivating technology can be…when it works.

Today I did my standard Starbucks out and back but my Garmin ran out of batteries while I was enjoying an iced tea. Then to make matters worse, my iPhone assumed that every 30 seconds I had hit the “Voice Command” button. I guess I sweat to much on the little headphone switch.

So I rode home without telemetry, tunes or much motivation.

Here’s part of it.

I went out for a brief run tonight after the gym…I still haven’t figured out why people are into it.

A little better than the last attempt.

On a lighter note 413 Calories would negate a McDouble with an extra ketchup packet.

I’m guessing it was the weather or maybe just being in a better mood but I just cranked out 15.99 miles in a touch over one hour on the bike.

I felt like I was dragging a little on the way out. I’m going to blame it on the gusty headwind. After sitting at Starbucks for a couple of minutes drinking a Green/Black tea I felt a little queasy. I hung out for a while and felt a bit better so I decided not to whimp out and take the Metro home. Besides, 18 Susan B. Anthony dollars would be kind of annoying. In hindsight I could have just gotten change at Starbuckies.

Anyway, I started rocking towards home and cranked it up a little. Maybe the gusty headwind was now a tail wind and maybe Hanley towards The River is sort of downhill but I moved my average speed of 15.23 on the way out to 15.77 for the entire ride. Booyeah…thats a fast ride for me.

My old Chase to Home time trial average speed from June 19 was 15.5mph over 3.5 miles.

It looks like all of my hard work is finally paying off. The scale read 224.8 this morning and I’m getting faster on the bike. I just have to work on running. No, I am not entering any triathlons…I’d hate to have to ride a bike with soggy shorts.

Check out the Laps on the detail page. There are a few above 18mph and one that almost kissed 19mph.

This morning I jumped on the scale and it read 224.8

I’ve reached my goal. Looking in the mirror with a critical eye I feel like i can lose another 25 pounds and actually see some abs.

I posted this on Facebook this morning and my buddy Dave, also a low-carb convert, issued a challenge. So we’re in a race to lose 25 pounds and have visible abs.

I will keep all of you posted with my progress and I am inviting Dave to do the same here on the paunchiness blog.

In case anyone is wondering how I went from 285 in April to 225 today, all of the answers are contained here. Proper nutrition, rigorous exercise (HIIT) and a bit of self loathing.

I don’t like to lose a good competition so get ready.

Biochemist proposes worldwide policy change to step up daily vitamin D intake

Vitamin D is effective in reducing frequency of many diseases and cost of medical care, stresses UC Riverside’s Anthony Norman

Anthony Norman, a leading international expert in vitamin D, proposes worldwide policy changes regarding people’s vitamin D daily intake amount in order to maximize the vitamin’s contribution to reducing the frequency of many diseases, including childhood rickets, adult osteomalacia, cancer, autoimmune type-1 diabetes, hypertension, cardiovascular disease, obesity and muscle weakness.

“A reduction in the frequency of these diseases would increase the quality and longevity of life and significantly reduce the cost of medical care worldwide,” said Norman, a distinguished professor emeritus of biochemistry and biomedical sciences at the University of California, Riverside. “It is high time that worldwide vitamin D nutritional policy, now at a crossroads, reflects current scientific knowledge about the vitamin’s many benefits and develops a sound vision for the future.”

Currently, the recommended daily intake of vitamin D in the United States is 200 international units (IU) for people up to 50 years old; 400 IU for people 51 to 70 years old; and 600 IU for people over 70 years old. Today there is a wide consensus among scientists that the relative daily intake of vitamin D should be increased to 2,000 to 4,000 IU for most adults.

“Worldwide public health is best served by a recommendation of higher daily intakes of vitamin D,” Norman said. “Currently, more than half the world’s population gets insufficient amounts of this vitamin. At present about half of elderly North Americans and Western Europeans and probably also of the rest of the world are not receiving enough vitamin D to maintain healthy bone.”

Reporting in a review paper in the July 28, 2010, issue of Experimental Biology and Medicine, Norman and Roger Bouillon of the Laboratory of Experimental Medicine and Endocrinology at the Katholieke Universiteit Leuven, Belgium, warn that if the current nutritional guidelines for vitamin D remain unchanged, rickets and osteomalacia, which could be easily prevented, will continue to occur.

They add that if the present guidelines for vitamin D intake are strictly implemented and applied worldwide to pregnant or lactating women, newborns and children, the occurrence of rickets in infants could be effectively eradicated.

Norman, the first author of the review paper, and Bouillon note that if the daily dietary intake of vitamin D is increased by 600-1000 IU in all adults above their present supply, it would bring beneficial effects on bone health in the elderly and on all major human diseases (e.g., cancer, cardiovascular, metabolic and immune diseases).

The researchers add, however, that if the vitamin D dietary intake were increased to 2000 IU per day and even more for subgroups of the world population with the poorest vitamin D status, it could favorably impact multiple sclerosis, type-1 diabetes, tuberculosis, metabolic syndrome, cardiovascular risk factors and most cancers.

About vitamin D:

Also known as the “sunshine vitamin,” vitamin D was discovered 90 years ago as a dietary agent that prevented the bone disease rickets.

Exposure to the sun is the body’s natural way of producing the vitamin. Skin exposed to solar UVB radiation can produce significant quantities of vitamin D. But this vitamin D synthesis is reliably available year-round only at latitudes between 40 degrees north and 40 degrees south. A combination of sunshine, food, supplements, and possibly even limited tanning exposure can raise the daily intake of the vitamin to 2000 IU.

Vitamin D is itself biologically inert. Its biological effects result only after it is metabolized first in the liver and then in the kidney – a process that converts the vitamin into a steroid hormone.

The best sources of unfortified foods naturally containing vitamin D are animal products and fatty fish and liver extracts like salmon or sardines and cod liver oil. Vitamin D-fortified food sources in the United States (the fortification levels aim at about 400 IU per day) include milk and milk products, orange juice, breakfast cereals and bars, grain products, pastas, infant formulas and margarines.

Vitamin D excess can cause health problems such as hypercalcemia, vomiting, thirst and tissue damage. The precise upper limit for daily vitamin D intake is not well defined.

I’ve got it in my head that I want to be a runner. I’ve tried this experiment a couple of times and at one point long ago ran a 5k in just under 25 minutes.

I bought some new shoes because the padding in my 993′s was shot and hit the proverbial bricks. Ouch…running hurts. I was pretty disappointed after these results:

A little under two miles in 25 minutes sort of sucks. In my defense this is the first time I’ve tried to run in over a year.

Last night I went out with the Garmin again and turned in similarly pathetic results:

Now, here’s where it gets interesting. If you look at the timing I suck, if you dig a little deeper then maybe I’m not so bad.

My average heart rate for 25 minutes of running and walking was 130 bpm. If you look at the chart you can see the little peaks that correspond to the peaks in speed. The slower speeds are when I was walking, higher speeds are running obviously. Here’s the interesting part. If you go back and look at Sunday Afternoon Ride you can see my average heart rate is 156 over the course of an hour. There are still peaks and valleys or times of exertion and rest. My point is that my cardiovascular health is such that I can maintain 85% of my maximum heart rate for an hour except when I’m running.

In summary, my excuse is that my problem is leg strength or more specifically muscle memory. Here’s what wikipedia has to say:

When participating in any sport, new motor skills and movement combinations are frequently being used and repeated. All sports require some degree of strength, endurance training and skilled reaching, in order to be successful in the required tasks.

[13] Specifically, strength training enhances motor neuron excitability and induces synaptogenesis, both of which would help in enhancing communication between the nervous system and the muscles themselves.^[13].

[14] This confirms that muscle strength is first influenced by the inner neural circuitry, rather than by external physiological changes in the muscle size.

[13] In addition, neurotropic factors within the motor cortex are upregulated in response to endurance training to promote neural survival.^[13]

[15] Even a small amount of training may be enough to induce neural processes that continue to evolve even after the training has stopped, which provides a potential basis for consolidation of the task. Additionally, studying mice while they are learning a new complex reaching task, has found that “motor learning leads to rapid formation of dendritic spines (spinogenesis) in the motor cortex contralateral to the reaching forelimb”.^[16] However, motor cortex reorganization itself does not occur at a uniform rate across training periods. It has been suggested that the synaptogenesis and motor map reorganization merely represent the consolidation, and not the acquisition itself, of a specific motor task.^[17] Furthermore, the degree of plasticity in various locations (namely motor cortex versus spinal cord) is dependent on the behavioural demands and nature of the task (i.e. skilled reaching versus strength training).^[13]

[13] Strength training results are seen in the spinal cord well before any physiological muscular adaptation is established through muscle hypertrophy or atrophy.^[13] The results of endurance and strength training, and skilled reaching, therefore combine to help each other maximize performance output.

Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet

A Randomized Trial

Gary D. Foster, PhD; Holly R. Wyatt, MD; James O. Hill, PhD; Angela P. Makris, PhD, RD; Diane L. Rosenbaum, BA; Carrie Brill, BS; Richard I. Stein, PhD; B. Selma Mohammed, MD, PhD; Bernard Miller, MD; Daniel J. Rader, MD; Babette Zemel, PhD; Thomas A. Wadden, PhD; Thomas Tenhave, PhD; Craig W. Newcomb, MS; and Samuel Klein, MD

Background: Previous studies comparing low-carbohydrate and low-fat diets have not included a comprehensive behavioral treatment, resulting in suboptimal weight loss.

Objective: To evaluate the effects of 2-year treatment with a low-carbohydrate or low-fat diet, each of which was combined with a comprehensive lifestyle modification program.

Design: Randomized parallel-group trial. (ClinicalTrials.gov registration number: NCT00143936)

Setting: 3 academic medical centers.

Patients: 307 participants with a mean age of 45.5 years (SD, 9.7 years) and mean body mass index of 36.1 kg/m2 (SD, 3.5 kg/m2).

Intervention: A low-carbohydrate diet, which consisted of limited carbohydrate intake (20 g/d for 3 months) in the form of low–glycemic index vegetables with unrestricted consumption of fat and protein. After 3 months, participants in the low-carbohydrate diet group increased their carbohydrate intake (5 g/d per wk) until a stable and desired weight was achieved. A low-fat diet consisted of limited energy intake (1200 to 1800 kcal/d; ≤30% calories from fat). Both diets were combined with comprehensive behavioral treatment.

Measurements: Weight at 2 years was the primary outcome. Secondary measures included weight at 3, 6, and 12 months and serum lipid concentrations, blood pressure, urinary ketones, symptoms, bone mineral density, and body composition throughout the study.

Results: Weight loss was approximately 11 kg (11%) at 1 year and 7 kg (7%) at 2 years. There were no differences in weight, body composition, or bone mineral density between the groups at any time point. During the first 6 months, the low-carbohydrate diet group had greater reductions in diastolic blood pressure, triglyceride levels, and very-low-density lipoprotein cholesterol levels, lesser reductions in low-density lipoprotein cholesterol levels, and more adverse symptoms than did the low-fat diet group. The low-carbohydrate diet group had greater increases in high-density lipoprotein cholesterol levels at all time points, approximating a 23% increase at 2 years.

Limitation: Intensive behavioral treatment was provided, patients with dyslipidemia and diabetes were excluded, and attrition at 2 years was high.

Conclusion: Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years.

I decided to take it easy for today’s ride. I loped along at about 12 mph and kept my heart rate low.

To upload your ride or run stats to Garmin check out the 405CX

Garmin Forerunner 405CX GPS Sport Watch with Heart Rate Monitor (Blue)
Price: 0.00

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The Forerunner 405CX is the evolution of GPS-enabled training. This sleek sport watch tracks your distance, pace and heart rate, then wirelessly sends the data to your PC for later analysis. The 405CX features heart rate-based calorie computation and comes with a second wrist band option suitable for smaller wrists.

The evolution of GPS-enabled training.

Continuously records your time, distance, pace, calories burned and heart rate. Click to enlarge.

Transfer data to your computer when Forerunner is in range–no cables, no hookups. Click to enlarge.

Watch Results
Loaded with serious training features, Forerunner 405CX continuously records your time, distance, pace, calories burned and heart rate. Each workout is stored in memory so you can review and analyze the data to see how you’ve improved. And advanced training features will challenge you to step up your pace–race against Forerunner’s Virtual Partner to improve your times, or set up interval workouts without having to circle the track. You can even download recorded courses to compete against previous workouts. To use the watch, simply tap the touch bezel to change screens without fumbling for a button.

Track Heart Rate
Forerunner 405CX comes with a flexible, wireless heart rate monitor to help you make the most out of your training. The digital heart rate monitor continuously tracks heart beats per minute and uses your heart rate for advanced calorie computation, so you know how many calories you’re burning. Train in a certain heart rate zone to improve your fitness level or compare your pace and heart rate to past performance on the same run.

Share Workouts Wirelessly
With Forerunner 405CX, you can share your locations, advanced workouts and courses wirelessly with other Forerunner 405 users. Send your favorite workout to your friends to try, or compete against someone else’s recorded course. Sharing data is easy: just select “transfer” to send your information to a nearby device.

Run, Sync, Store and Share
Once you’ve logged the miles, innovative ANT+ wireless technology automatically transfers data to your computer when Forerunner is in range. No cables, no hookups. The data’s just there, ready for you to analyze, categorize and share through our online community, Garmin Connect or our optional Garmin Training Center software. You can even plan workouts on your computer and then send them to your Forerunner.

Train Year Round
Take your training inside with the versatile Forerunner 405CX and optional wireless accessories. Pair it with an optional foot pod to track your speed, distance and running cadence indoors when GPS signals are unavailable. The wireless foot pod clips onto your laces for easy removal and automatically turns on when you start moving. Or pair your Forerunner with an optional speed/cadence bike sensor to track the speed and distance of your cycling workouts.

What’s in the Box
Forerunner 405CX, USB ANT stick, Heart rate monitor, Two additional wrist straps, AC charger, Charging clip, Owner’s manual on disk, Quick reference guide

Garmin Forerunner 405CX GPS Sport Watch with Heart Rate Monitor (Blue)
Price: 0.00

35 used & new available from 283.99

The weather was finally cool enough for a nice ride.

Today someone caught me eating cheese. I got a disappointed look that said “you’ve come so far, don’t screw it up now.”

So, I opened up my browser and Googled saturated fat. Here’s what Men’s Health had to say:

What if Bad Fat is Actually Good for You?

For decades, Americans have been told that saturated fat clogs arteries and causes heart disease. But there’s just one problem: No one’s ever proved it

Suppose you were forced to live on a diet of red meat and whole milk. A diet that, all told, was at least 60 percent fat — about half of it saturated. If your first thoughts are of statins and stents, you may want to consider the curious case of the Masai, a nomadic tribe in Kenya and Tanzania.

In the 1960s, a Vanderbilt University scientist named George Mann, M.D., found that Masai men consumed this very diet (supplemented with blood from the cattle they herded). Yet these nomads, who were also very lean, had some of the lowest levels of cholesterol ever measured and were virtually free of heart disease.

Scientists, confused by the finding, argued that the tribe must have certain genetic protections against developing high cholesterol. But when British researchers monitored a group of Masai men who moved to Nairobi and began consuming a more modern diet, they discovered that the men’s cholesterol subsequently skyrocketed.

Similar observations were made of the Samburu — another Kenyan tribe — as well as the Fulani of Nigeria. While the findings from these cultures seem to contradict the fact that eating saturated fat leads to heart disease, it may surprise you to know that this “fact” isn’t a fact at all. It is, more accurately, a hypothesis from the 1950s that’s never been proved.

The first scientific indictment of saturated fat came in 1953. That’s the year a physiologist named Ancel Keys, Ph.D., published a highly influential paper titled “Atherosclerosis, a Problem in Newer Public Health.” Keys wrote that while the total death rate in the United States was declining, the number of deaths due to heart disease was steadily climbing. And to explain why, he presented a comparison of fat intake and heart disease mortality in six countries: the United States, Canada, Australia, England, Italy, and Japan.

The Americans ate the most fat and had the greatest number of deaths from heart disease; the Japanese ate the least fat and had the fewest deaths from heart disease. The other countries fell neatly in between. The higher the fat intake, according to national diet surveys, the higher the rate of heart disease. And vice versa. Keys called this correlation a “remarkable relationship” and began to publicly hypothesize that consumption of fat- causes heart disease. This became known as the diet-heart hypothesis.

At the time, plenty of scientists were skeptical of Keys’s assertions. One such critic was Jacob Yerushalmy, Ph.D., founder of the biostatistics graduate program at the University of California at Berkeley. In a 1957 paper, Yerushalmy pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, statistics were actually available for 22 countries. And when all 22 were analyzed, the apparent link between fat consumption and heart disease disappeared. For example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.
The other salient criticism of Keys’s study was that he had observed only a correlation between two phenomena, not a clear causative link. So this left open the possibility that something else — unmeasured or unimagined — was leading to heart disease. After all, Americans did eat more fat than the Japanese, but perhaps they also consumed more sugar and white bread, and watched more television.

Despite the apparent flaws in Keys’s argument, the diet-heart hypothesis was compelling, and it was soon heavily promoted by the American Heart Association (AHA) and the media. It offered the worried public a highly educated guess as to why the country was in the midst of a heart-disease epidemic. “People should know the facts,” Keys said in a 1961 interview with Time magazine, for which he appeared on the cover. “Then if they want to eat themselves to death, let them.”

The seven-countries study, published in 1970, is considered Ancel Keys’s landmark achievement. It seemed to lend further credence to the diet-heart hypothesis. In this study, Keys reported that in the seven countries he selected — the United States, Japan, Italy, Greece, Yugoslavia, Finland, and the Netherlands — animal-fat intake was a strong predictor of heart attacks over a 5-year period. Just as important, he noted an association between total cholesterol and heart-disease mortality. This prompted him to conclude that the saturated fats in animal foods — and not other types of fat — raise cholesterol and ultimately lead to heart disease.

Naturally, proponents of the diet-heart hypothesis hailed the study as proof that eating saturated fat leads to heart attacks. But the data was far from rock solid. That’s because in three countries (Finland, Greece, and Yugoslavia), the correlation wasn’t seen. For example, eastern Finland had five times as many heart-attack fatalities and twice as much heart disease as western Finland, despite only small differences between the two regions in animal-fat intake and cholesterol levels. And while Keys provided that raw data in his report, he glossed over it as a finding. Perhaps a larger problem, though, was his assumption that saturated fat has an unhealthy effect on cholesterol levels.

Although more than a dozen types of saturated fat exist, humans predominantly consume three: stearic acid, palmitic acid, and lauric acid. This trio comprises almost 95 percent of the saturated fat in a hunk of prime rib, a slice of bacon, or a piece of chicken skin, and nearly 70 percent of that in butter and whole milk.

Today, it’s well established that stearic acid has no effect on cholesterol levels. In fact, stearic acid — which is found in high amounts in cocoa as well as animal fat –i s converted to a monounsaturated fat called oleic acid in your liver. This is the same heart-healthy fat found in olive oil. As a result, scientists generally regard this saturated fatty acid as either benign or potentially beneficial to your health.
Palmitic and lauric acid, however, are known to raise total cholesterol. But here’s what’s rarely reported: Research shows that although both of these saturated fatty acids increase LDL (“bad”) cholesterol, they raise HDL (“good”) cholesterol just as much, if not more. And this lowers your risk of heart disease. That’s because it’s commonly believed that LDL cholesterol lays down plaque on your artery walls, while HDL removes it. So increasing both actually reduces the proportion of bad cholesterol in your blood to the good kind. This may explain why numerous studies have reported that this HDL/LDL ratio is a better predictor of future heart disease than LDL alone.

All of this muddies Keys’s claim of a clear connection between saturated-fat intake, cholesterol, and heart disease. If saturated fat doesn’t raise cholesterol in such a way that it increases heart-disease risk, then according to the scientific method, the diet-heart hypothesis must be rejected. However, in 1977 it was still a promising idea.

That was the year Congress made it government policy to recommend a low-fat diet, based primarily on the opinions of health experts who supported the diet-heart hypothesis. It was a decision met with much criticism from the scientific community, including the American Medical Association. After all, officially endorsing a low-fat diet could change the eating habits of millions of Americans, and the potential effects of this strategy were widely debated and certainly unproved.

We’ve spent billions of our tax dollars trying to prove the diet-heart hypothesis. Yet study after study has failed to provide definitive evidence that saturated-fat intake leads to heart disease. The most recent example is the Women’s Health Initiative, the government’s largest and most expensive ($725 million) diet study yet. The results, published last year, show that a diet low in total fat and saturated fat had no impact in reducing heart-disease and stroke rates in some 20,000 women who had adhered to the regimen for an average of 8 years.

But this paper, like many others, plays down its own findings and instead points to four studies that, many years ago, apparently did find a link between saturated fat and heart disease. Because of this, it’s worth taking a closer look at each.

The Los Angeles VA Hospital Study (1969) This UCLA study of 850 men reported that those who replaced saturated fats with polyunsaturated fats were less likely to die of heart disease and stroke over a 5-year period than were men who didn’t alter their diets. However, more of those who changed their diets died of cancer, and the average age of death was the same in both groups. What’s more, “through an oversight,” the study authors neglected to collect crucial data on smoking habits from about 100 men. They also reported that the men successfully adhered to the diet only half the time.

The Oslo Diet-Heart Study (1970) Two hundred men followed a diet low in saturated fat for 5 years while another group ate as they pleased. The dieters had fewer heart attacks, but there was no difference in total deaths between the two groups.

The Finnish Mental Hospital Study (1979) This trial took place from 1959 to 1971 and appeared to document a reduction in heart disease in psychiatric patients following a “cholesterol-lowering” diet. But the experiment was poorly controlled: Almost half of the 700 participants joined or left the study over its 12-year duration.
The St. Thomas’ Atherosclerosis Regression Study (1992) Only 74 men completed this 3-year study conducted at St. Thomas’ Hospital, in London. It found a reduction in cardiac events among men with heart disease who adopted a low-fat diet. There’s a major caveat, though: Their prescribed diets were also low in sugar.

These four studies, even though they have serious flaws and are tiny compared with the Women’s Health Initiative, are often cited as definitive proof that saturated fats cause heart disease. Many other more recent trials cast doubt on the diet-heart hypothesis. These studies should be considered in the context of all the other research.

In 2000, a respected international group of scientists called the Cochrane Collaboration conducted a “meta-analysis” of the scientific literature on cholesterol-lowering diets. After applying rigorous selection criteria (219 trials were excluded), the group examined 27 studies involving more than 18,000 participants. Although the authors concluded that cutting back on dietary fat may help reduce heart disease, their published data actually shows that diets low in saturated fats have no significant effect on mortality, or even on deaths due to heart attacks.

“I was disappointed that we didn’t find something more definitive,” says Lee Hooper, Ph.D., who led the Cochrane review. If this exhaustive analysis didn’t provide evidence of the dangers of saturated fat, says Hooper, it was probably because the studies reviewed didn’t last long enough, or perhaps because the participants didn’t lower their saturated-fat intake enough. Of course, there is a third possibility, which Hooper doesn’t mention: The diet-heart hypothesis is incorrect.

Ronald Krauss, M.D., won’t say saturated fats are good for you. “But,” he concedes, “we don’t have convincing evidence that they’re bad, either.”

For 30 years, Dr. Krauss — an adjunct professor of nutritional sciences at the University of California at Berkeley — has been studying the effect of diet and blood lipids on cardiovascular disease. He points out that while some studies show that replacing saturated fats with unsaturated fats lowers heart-disease risk, this doesn’t mean that saturated fats lead to clogged arteries. “It may simply suggest that unsaturated fats are an even healthier option,” he says.

But there’s more to this story: In 1980, Dr. Krauss and his colleagues discovered that LDL cholesterol is far from the simple “bad” particle it’s commonly thought to be. It actually comes in a series of different sizes, known as subfractions. Some LDL subfractions are large and fluffy. Others are small and dense. This distinction is important.

A decade ago, Canadian researchers reported that men with the highest number of small, dense LDL subfractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. These findings were confirmed in subsequent studies.

Now here’s the saturated-fat connection: Dr. Krauss found that when people replace the carbohydrates in their diet with fat–saturated or unsaturated — the number of small, dense LDL particles decreases. This leads to the highly counterintuitive notion that replacing your breakfast cereal with eggs and bacon could actually reduce your risk of heart disease.
Men, more than women, are predisposed to having small, dense LDL. However, the propensity is highly flexible and, according to Dr. Krauss, can be switched on when people eat high-carb, low-fat diets or switched off when they reduce carbs and eat diets high in fat, including the saturated variety. “There’s a subgroup of people at high risk of heart disease who may respond well to diets low in fat,” says Dr. Krauss. “But the majority of healthy people seem to derive very little benefit from these low-fat diets, in terms of heart-disease risk factors, unless they also lose weight and exercise. And if a low-fat diet is also loaded with carbs, it can actually result in adverse changes in blood lipids.”

While Dr. Krauss is much published and highly respected — he has served twice as chairman of the writing committee of the AHA’s dietary guidelines — the far-reaching implications of his work have not been generally acknowledged. “Academic scientists believe saturated fat is bad for you,” says Penny Kris-Etherton, Ph.D., a distinguished professor of nutritional studies at Penn State University, citing as evidence the “many studies” she believes show it to be true. But not everyone accepts those studies, and their proponents find it hard to be heard. Kris-Etherton acknowledges that “there’s a good deal of reluctance toward accepting evidence suggesting the contrary.”

Take, for example, a 2004 Harvard University study of older women with heart disease. Researchers found that the more saturated fat these women consumed, the less likely it was their condition would worsen. Lead study author Dariush Mozaffarian, Ph.D., an assistant professor at Harvard’s school of public health, recalls that before the paper was published in the American Journal of Clinical Nutrition, he encountered formidable politics from other journals.

“In the nutrition field, it’s very difficult to get something published that goes against  established dogma,” says Mozaffarian. “The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence.” Mozaffarian says he believes it’s critical that scientists remain open minded. “Our finding was surprising to us. And when there’s a discovery that goes against what’s established, it shouldn’t be suppressed but rather disseminated and explored as much as possible.”

Perhaps the apparent bias against saturated fat is most evident in studies on low-carbohydrate diets. Many versions of this approach are controversial because they place no limitations on saturated-fat intake. As a result, supporters of the diet-heart hypothesis have argued that low-carb diets will increase the risk of heart disease. But published research doesn’t show this to be the case. When people on low-carb diets have been compared head-to-head with those on low-fat diets, the low-carb dieters typically scored significantly better on markers of heart disease, including small, dense LDL cholesterol, HDL/LDL ratio, and triglycerides, which are a measure of the amount of fat circulating in your blood.

For example, in a new 12-week study, University of Connecticut scientists placed overweight men and women on either a low-carb or low-fat diet. Those who followed the low-carb diet consumed 36 grams of saturated fat per day (22 percent of total calories), which represented more than three times the amount in the low-fat diet. Yet despite this considerably greater intake of saturated fat, the low-carb dieters reduced both their number of small, dense LDL cholesterol and their HDL/LDL ratio to a greater degree than those who ate a low-fat diet. In addition, triglycerides decreased by 51 percent in the low-carb group–compared with 19 percent in the low-fat group.
This finding is worth noting, because even though cholesterol is the most commonly cited risk factor for heart disease, triglyceride levels may be equally relevant. In a 40-year study at the University of Hawaii, scientists found that low triglyceride levels at middle age best predicted “exceptional survival” — defined as living until age 85 without suffering from a major disease.

According to lead study author Jeff Volek, Ph.D., R.D., two factors influence the amount of fat coursing through your veins. The first, of course, is the amount of fat you eat. But the more important factor is less obvious. Turns out, your body makes fat from carbohydrates. It works like this: The carbs you eat (particularly starches and sugar) are absorbed into your bloodstream as sugar. As your carb intake rises, so does your blood sugar. This causes your body to release the hormone insulin. Insulin’s job is to return your blood sugar to normal, but it also signals your body to store fat. As a result, your liver starts converting excess blood sugar to triglycerides, or fat.

All of which helps explain why the low-carb dieters in Volek’s study had a greater loss of fat in their blood. Restricting carbs keeps insulin levels low, which lowers your internal production of fat and allows more of the fat you do eat to be burned for energy.

Yet even with this emerging data and the lack of scientific support for the diet-heart hypothesis, the latest AHA dietary guidelines have reduced the recommended amount of saturated fat from 10 percent of daily calories to 7 percent or less. “The idea was to encourage people to decrease their saturated-fat intake even further, because there’s a linear relationship between saturated-fat intake and LDL cholesterol,” says Alice H. Lichtenstein, Ph.D., Sc.D., who led the AHA nutrition committee that wrote the recommendation.

What about Krauss’s findings that not all LDL is equal? Lichtenstein says that her committee didn’t address them, but that it might in the future.

It could be that it’s not bad foods that cause heart disease, it’s bad habits. After all, in Volek’s study, participants who followed the low-fat diet — which was high in carbs — also decreased their triglycerides. “The key factor is that they weren’t overeating,” says Volek. “This allowed the carbohydrates to be used for energy rather than converted to fat.” Perhaps this is the most important point of all. If you consistently consume more calories than you burn, and you gain weight, your risk of heart disease will increase — whether you favor eating saturated fats, carbs, or both.

But if you’re living a healthy lifestyle — you aren’t overweight, you don’t smoke, you exercise regularly — then the composition of your diet may matter much less. And, based on the research of Volek and Dr. Krauss, a weight-loss or maintenance diet in which some carbohydrates are replaced with fat — even if it’s saturated — will reduce markers of heart-disease risk more than if you followed a low-fat, high-carb diet.

“The message isn’t that you should gorge on butter, bacon, and cheese,” says Volek. “It’s that there’s no scientific reason that natural foods containing saturated fat can’t, or shouldn’t, be part of a healthy diet.”

For more on this topic and a guide to foods you shouldn’t fear, check out “Fat Foods You Can Eat”.

Check out laps 13-15 on the flats of Lindell…Booyeah

I got on the bike yesterday with the intention of logging some miles towards my 50 mile goal for the week. It was windy. I called it quits after 4 miles. Actually, I called it quits after 2 miles and had to ride home.

Lets just say that my average heart rate was 140 instead of 115 or so and my cadence was around 85rpm but my average speed was only a few tenths faster than the 10mph wind.

I went out for a leisurely ride this morning. It looks like I am actually making some progress my average speed for the first 9 miles was 12.6 mph. That’s only 3mph slower than last weeks Chase to home 3.5 mile ride. I have also officially lost 50 pounds.

Go me.

Chase to Home – June 19, 2010

Chase to Home – May 12, 2010

Bacon Potato Chips

At Atomicdust, we have a slight obsession with the television series Lost. The fact that we have more than one image of John Locke hanging around our office should be proof enough, but just in case you’re not sold…

Matt, our resident Lost expert, not only hosts finale parties at the end of each season, but he comes up with invitations, decorations, and videos to accompany them.

That’s right, we said videos.

This isn’t your typical fan video from YouTube. This is not images of Kate and Jack (or Kate and Sawyer, or Sawyer and Juliet or…) set to ‘Endless Love.’ This video has a plot, ‘acting’, and parts of it were even filmed on location in Costa Rica.

Just in time for the big premiere tonight, Matt has released Part One of the Season 6 Finale Video on his blog Matt’s Lost His Mind!

Check it out (and make sure to look for Atomicdust-ers Mike and Matt in starring roles!):
Part One of the LOST Season 6 Finale Video

I got home from work today and I was feeling pretty lazy. I plopped down on the couch and grabbed the remote. I looked to my right and saw the rowing machine staring at me. I didn’t want to get on it, but I had felt that way yesterday and the day before too.

I half heartedly strapped my feet in and began to row.

I only expected to do 10 minutes but I kept pushing and cranked out a full twenty. I actually felt better.

I guess the trick is to just do it. exercise invigorates the mind and body, or so they say…I do actually feel a bit more energetic.

get out there and get on it.

A business trip and a late night pizza commercial derailed me for a bit last week. I got back on it and just crossed the 270 threshold to 269.

If you haven’t read the New York Times Magazine article about low carb dieting here’s a link…

My Ketostix are officially turning pink again.

here’s a recipe for low carb Italian beef.

5lbs beef roast
1/2 jar pepperchinni
5 cloves garlic
1 sm package fresh basil
2 tsp salt

put all of this in a crockpot or a saucepan over low heat and cook for at least three hours. shred with tongs or a fork. Your non low carb friends can eat it on a baguette or rye bread.

Homer Simpson would squeal with delight

Starting tomorrow, the folks at The Wine & Cheese Place will launch a major offensive in the war against vegetarianism. More specifically, they’ll announce the first artisan bacon to be featured in what they deem “the year of the BACON at TWCP.”

But this is just the beginning: TWCP has huge plans, as you may have gathered from the quote. Monthly (or more frequently, depending on demand – c’mon, biweekly!), the stores will feature a new and different artisan bacon in what’s basically a bacon-of-the-month club … except you don’t have to sign up for anything, do any research or pay shipping costs. All you have to do is arrive in time to buy some before it sells out.

According to TWCP, the fastest and surest way to get details is through its blog or Facebook page. As for the bacon to be announced Wednesday? It sounds like a very worthy debut; this will be its initial offering in St. Louis, and it’s gotten rave reviews elsewhere. Otherwise, I’m not telling – because I want to be first in line.

– Dennis Lowery

Via Sauce Magazine

I’ll be there…

Globo Gym Commercial from Dodgeball
Tired of the same old you? Tired of being out of shape and out of luck with the opposite sex? Tired of being overweight and under-attractive?

Yeah! Oh, hello. I’m White Goodman, Owner, Operator, and Founder of Globo Gym America Corp, and I’m here to tell you that you don’t have to be stuck with what ya got.

Here at Globo Gym, we understand that “Ugliness” and “Fatness” are genetic disorders, much like baldness or necrophilia, and it’s only your fault if you don’t hate yourself enough to do something about it.

And that’s where we come in.

Globo Gym employs a highly-trained, quasi-cultural staff of personal alterational specialists. And with our competitively-priced on-site cosmetic surgery, we can turn that Frankenstein you see in the mirror every morning into a Franken-fine!

Of course you’ll still be you in a legal sense, but think of it as a thinner, more attractive, better you than you could ever become without us. How do I know? Well, I’m not only the founder of Globo Gym. I’m also a client.

That’s me. Six years and 600 pounds ago… before I knew how much I hated myself. But that all changed once I founded Globo Gym. But don’t just take my word for it. Listen to these Globo-Gymers tell you how it is.

Someone asked me what my motivation was… I think this scene from Dodgeball pretty much sums it up, “it’s only your fault if you don’t hate yourself enough to do something about it.”