27 November 2008

Diet Update - Getting Past a Plateau

It has been a year since I got gout (right before Thanksgiving, 2007). The gout prompted me to start studying my diet in depth and for the first time in my life learn about what I put into my body. I went on a generally lower carbohydrate diet and wrote about my successes and findings in the following posts:


In all of those posts I have advocated a lower carbohydrate approach.

It has been a year now and I wanted to report on where I am now and what additional learnings I have.

This graphic shows my progress since early 2007. You can see the change in slope when I got gout, learned about diet and went onto a lower carb/paleo diet track. I hit a plateau in May of 2008 at 206 pounds and so I went on Lyle McDonald's Rapid Fat Loss Protocol, a "Protein Sparing Modified Fast" or PSMF method. On that I lost about 6 pounds in three weeks, then carried that momentum down to 196 pounds. My initial goal was to get to 200 pounds.

You can also see that since my low point in about August, I have rebounded a bit, but fluctuated around 200 lbs. Unfortunately, 200 is no longer my goal. I hope to continue on down to maybe 180, then drift up a little to 185 or so for maintenance. So what's going on? Why did the weight loss stop?
First, some rebound (5 pounds or so) is very common as people go off a low carb diet. On low carb, the body depletes glycogen and water in the muscles and liver causing a rapid 5 - 10 pound loss. Coming off low carb simply reverses that. This comes off fast when you go back onto low carb, so is of little concern. That's what happened to me in October of 2008 when I went from 205 to about 197.

However, I am having trouble now progressing to my new goal. Here are some of the issues I think I have.

1. Goal Clarity - Once I hit 200 I started thinking about putting on some more muscle. I ramped up my workouts and started to eat more. My weightlifting increased pretty quickly, but so did my weight. It might have been some muscle, but there was also some fat. I hated giving up the loss and felt a bit conflicted about it. So I went back onto the PSMF--for about a week. The weight came off fast, but then life stepped in and I exercised less, ate more and put the weight right back on. This brings us to the next issue.

2. Motivation - Once you state a goal, you have to maintain focus on it and keep at it. Losing weight really is harder than maintaining it. As you approach your goal it gets even harder for a number of reasons including the fact that you are losing fat, which changes your hormonal environment.

This blog has a good write up about motivation. As you get to a place that is adequate, you may feel tempted to slack off. That is part of my problem right now. I'm pretty happy about losing 35 lbs., blood markers and health are much better, etc. Sometimes artificial motivation can help (like an artificial deadline at the office). Stickk.com provides a place to build that artificail motivation. You can place a bet or a challenge with friends and have referees to check. you can set goals with penalties for missing checkpoints. Perhaps you could set it up to send a check to a cause with which you do not agree.

3. Stick with what got you there - Moving from diet to maintenance will stop your weight loss. If you want to lose weight again, you have to make changes. Going with what got you there (whether Atkins, Paleo, Weight Watchers) in the first place is a good place to start. The ladies who write this blog also have a book about maintaining weight loss called Refuse to Regain (link below).

4. Don't stick with what got you there - As you get to lower levels of body fat (less than 12% for men or 18% for women) Lyle McDonald has written a really good series (1) (2) (3) (4) (5) (6) about the impact of leptin on weight loss. Leptin is a hormone that is created in your fat and can help you lose weight. As your fat decreases you secrete less leptin. It's one of several reasons you may have to make changes. He also has a book called The Stubborn Fat Solution, which covers a program to cut that last bit of fat. It's not for everyone, but if you are at that lower level of fat, you might consider it.

I am continuing on. I have ramped up my exercise to maintain strength and assist with fat loss, and I am going back to a stricter diet. My goal is still to get down to a maintenance range of 180-185 or so.

I still believe that a lower carb approach is better for me, and probably healthier for most people. If you haven't tried eating lower carb, I encourage you to try. I think that Protein Power, Atkins, or Paleo diet approaches (links below) are all potentially good programs.

However, there are a number of variables that can affect how people respond. Some people simply can't get past the "brain fog" that temporarily occurs during adaptation to low carb. Specific goals, activity levels, age, sex, and biochemical makeup all affect what you should be doing to eat right.


Good luck and Happy Thanksgiving.









The following link is to a tool that can help you measure your progress on the road to better health.

11 November 2008

More Statin Misreporting

You may have read the breathless reporting on November 10 and 11, 2008.

From the San Francisco Chronicle

"A large new study, disclosed this week at a scientific meeting of the American Heart Association in New Orleans, found that even among people who appear to be in good health with relatively low cholesterol, the blood test could be a strong gauge of heart disease or stroke risk. If the test detects a high level of a specific protein, patients could reduce their risk of heart disease by using popular statin drugs, the study found.

"This kind of study probably will change cardiac practice," said Dr. Deepak Srivastava, director of the Gladstone Institute of Cardiovascular Disease at UC San Francisco. "The test will likely become part of the panels that are routinely done. The study provides pretty compelling evidence that even if people have normal cholesterol levels, then they would benefit from statins if they have signs of increased inflammation."

The Emotions For Engineers Take on the Study

A more accurate story would be something like,

A small percentage of the population with unusual blood indicators and already at low risk of total mortality can reduce their risk by about 0.5% by taking Crestor in the short-term. The long-term effects remain untested. Only those who do not have immediate side-effects may benefit.

This study effectively disproves the cholesterol hypothesis of heart disease. Although incidence of heart attacks and strokes was higher in the placebo group than in the test group, total mortality from these causes was the same.


It is important to note that very careful screening was done to reduce the number of confounding effects of the study. While this led to more successful outfcomes, it also limits the applicability of the study.
Before the study was cut short, there were indications of increased diabetes in the test group. Some reports have said that C-Reactive Protein is the cause of heart disease, but it is more likely an indicator, same as various cholesterol levels, visceral obesity, and high blood pressure.



In a nutshell, even though the study showed that for 8900 people with an unusual and very specific blood profile and screened medical histories, taking Crestor for a year and a half will delay 49 deaths. That's a good thing probably. It is tough to generalize this for several reasons.


1. The study was terminated early. Long-term effects of statins can be harsh, but did not have time to show up.
2. Very specific filters were applied to the people in the study including age, family history, blood markers, etc.
3. Elimination of people who had very early negative responses to the statins.
4. 25% of the statin group stopped taking the medicine. How did this impact the results? How were they included or not in the findings.
5. There are several conflicts of interest, which may or may not be meaningful, but are of note.

More information and opinions:

Crestor Side Effects from Dr. Duane Graveline, author of Statin Drugs Side Effects and the Misguided War on Cholesterol

"...Suddenly, increased numbers of rhabdomyolysis reports began to surface in Crestor users associated with secondary kidney damage and a more ominous threat of specific primary renal toxicity as well and the necessity to issue emergency warnings advising doctors to exercise special caution in the use of this drug with hypothyroidism, renal insufficiency, Asian sub-population groups and cyclosporine and gemfibrozil takers. Not a terribly auspicious welcome for Crestor, this new statin drug known for strength in a market already dominated by other powerful statins.

"Crestor is just another strong statin, using the same mechanisms as the others and having all the inherent potential for side effects. My books tell of the inevitable harm to the mevalonate tree by statins but that was the only way drug company biochemists could inhibit cholesterol so they did it anyhow, regardless of the potential for collateral damage. Does this action reflect sound judgment? They knew that inhibiting cholesterol at this point would also inhibit CoQ10, dolichols, normal phosphorylation and selenoprotein. Every doctor once knew this for they were taught it in medical school but few have bothered to review what mevalonate inhibition really means. In my books I refer to this as "girding" of the mevalonate tree.

"We have now learned much more about the side effects of Crestor. We have learned that cognitive, muscle and nerve problems, due to the inevitable impairment of glial cell cholesterol synthesis and mevalonate blockade are only part of the problem. The Crestor side effect potential, that it shares with all other statins, is far more basic than this. Now we have learned that mitochondria are an inevitable target of statins. Because of inhibition of CoQ10 availability with its powerful anti-oxidant effect, mitochondria are left fully exposed to the mutagenic effect of free radicals. The resulting mutations of mitochondria are what is causing the legions of permanent, disabling side effects.

"Permanent neuropathy, permanent myopathy, chronic neuromuscular degeneration, and Parkinsonism and ALS-like cases now are thought by some to be the result of permanent statin-induced, mitochondrial damage. Furthermore, the inherent ability of the body to identify and correct the daily load of mutations is impaired because of the previously unrecognized effect of dolichol inhibition from the earlier mevalonate blockade. If this is beginning to sound like a domino effect, you are right. We still are seeing the dominos topple one by one as time goes by - the result of marketing a class of drugs before it was fully investigated.

"Dolichols are vital to the synthesis of glycoproteins, which in addition to thousands of other duties must serve in this identification and correction of DNA damage role. Glycohydrolases, a member of the glycoprotein family of molecules is vital to this function. Five years ago we hardly knew what dolichols were and now we find them involved in so many unexpected places. So I must bring to your attention that Crestor shares all this with the other statins. Its potential for damage goes far beyond the original suspicions

[E4E note: Whatever that all means...]



From The Heartscan Blog
Crestor 20 mg per day, contrary to the study and to many statin studies, will not be tolerated for long by the majority. Muscles aches are not common--they are inevitable, sometimes incapacitating. While JUPITER showed 15% of both treatment and placebo groups experienced muscle effects--no different--this is wildly contrary to real life.


From HyperLipid

What the JUPITER study found was that in people with low cholesterol levels but elevated hsCRP levels, taking a statin dropped the overall mortality from low to a bit lower.

Bodycounts were 198/8901 in the statin group and 247/8901 in the placebo group. Clearly treating 8901 people for a year and a half will prevent 49 deaths. According to the lipid hypothesis, all of these lives saved should be as a result of less cardiovascular disease, such as fatal heart attacks.

He has some other great insights as well and a data table.



Junkfood Science - Exhaustive review analysis and critique of the study

Speculation from Dr Michael Eades, Author of Protein Power

..."Finally, the fishiest thing of all. They stopped the study right in the middle of it. When studies are done that might put people at risk by giving them potentially dangerous drugs, it is typical for an outside group to take a peek at the data at certain milestones to make sure the study medication isn’t killing people. When this data is evaluated, and it is found that subjects on the experimental medicine are dying at unacceptably high rates, the study is often halted. I’ve never seen a study halted because the placebo group was dying at higher rates. That really makes me wonder.

"One of the negative findings in this study was that the group on Crestor developed diabetes during the trial at a significantly higher rate than did those on placebo. I suspect that the outside group checked the progress of the study, found that the subjects on Crestor were at the time of the evaluation showing better results than those on placebo, so the decision was made to stop the study while it was looking good. Had it gone on for the full term, the deaths could have evened out, way more people could have developed diabetes, or who knows what might have occurred had the study continued. So, the powers that be decided to quit while ahead."

Mark Sisson of Mark's Daily Apple Sums It Up Best
"If anything, this study is just another bit of proof that total cholesterol and even total LDL are not the proximate cause of heart disease. Oxidation and resulting inflammation are. Furthermore, it suggests that reducing inflammation has a far greater benefit than reducing LDL cholesterol. I agree. So why won’t the medical establishment acknowledge this? The bigger question is: why would any doctor agree to prescribe a dangerous, expensive statin to the general public to save a few more lives by reducing inflammation (NOT by reducing cholesterol), when this could be far more easily and more significantly achieved (at far less cost, with far fewer side effects and with far greater effectiveness) with Omega 3-rich oils (I herein disclaim that I sell fish oil) and a few simple dietary adjustments like cutting back on grains and trans fats?
"The fact that the media has bought into this hype again reminds me to remind you that all health decisions are best left to the expert - in this case, it’s YOU. You know what to do."

Remember: Your health choices are yours. Educate yourself. Logic and science are a big part of medicine and your physical and emotional well-being. Just because your surgeonis good with his hands, it does not mean that he is worth squat when it comes to biochemistry. Make intelligent, informed choices. Don't go onto powerful drugs until other less intrusive approaches (like diet, exercise, sun, and sleep) have failed.