Lose weight and HDL goes . . . down

Steve started with a miserable HDL cholesterol of 27 mg/dl. As expected, the low HDL was associated with all its evil friends: small LDL, deficiency of healthy, large HDL, high triglycerides, VLDL, and a pre-diabetic blood sugar.

Steve committed to a strict diet of reduced processed carbohydrates like wheat products, reduced meat and saturated fats. He relied on vegetables, fruit, lean proteins, and healthy oils. Over a 6 month period, he lost an impressive 39 lbs. He proclaimed that he hadn't felt this good in 30 years.

We rechecked his HDL: 25 mg/dl.

"I don't get it!" Steve declared, understandably.

There's a curious phenomenon with HDL. If you lose weight, HDL goes up--but not right away. Steve had lost a substantial quantity of weight and was continuing to lose weight when the blood work was obtained. While HDL does indeed rise with weight loss, it doesn't do so immediately. In fact, in the first two or so months after significant weight lost, HDL goes down.

Why? I don't really have an explanation, but it is a very consistent effect.

Losing weight towards ideal weight is truly an effective strategy for raising HDL. But we need to be patient. If you've lost many pounds like Steve did, then waiting at least two months after weight has stabilized may be necessary to fully gauge the effect on raising HDL.

Comments (2) -

  • JT

    6/27/2007 9:00:00 PM |

    That is good to know.  I'm in the same boat as Steve with low HDL.  Just in the last week, my weight and body fat loss seem to have finally leveled off.  I'm hoping when I test again at the end of next month for my doctor, HDL will be up some – but if not this helps explain possibly why not.

  • buy generic viagra

    9/13/2010 6:01:29 AM |

    Loosing weight also help men with erection problem.. so it is always good in any way.

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Lipoprotein(a), menopause, and andropause

Lipoprotein(a), menopause, and andropause

Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.
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Is skinny necessary for reversal?

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

Comments (19) -

  • Nancy M.

    1/6/2008 9:25:00 PM |

    It all falls in line with obesity being another marker for an overall metabolic condition, not being the *cause* of the metabolic condition.  

    The biggest disservice the medical establishment has done is ignore the evidence of this and continue to prescribe a diet that just makes it all worse and worse.

    I'm glad you're spreading the good word!

  • Peter

    1/8/2008 1:32:00 PM |

    Hi Dr Davis,

    Another cracking post. It reminds me distinctly of a long discussion on Dr Bernstein's site as to whether weight loss to ideal weight is needed to normalise blood sugars in a type 2 diabetic. You appear to be looking at another aspect of the metabolic syndrome, IHD. And it appears to be quite obvious that weight loss, per se, is irrelevant to both IHD and normoglycaemia, PROVIDED you normalise the problems described as the metabolic syndrome.

    Furnham and fasting is equally interesting. One has to ask; what happens during fasting? A full water fast to might be expected to give up to a kilo of weight loss each week perhaps? I've never tried this, but would guess this is reasonable. With flat-line basal glucose and insulin levels. That's just under 150g/d of weight loss, of which perhaps at least 100g/d is body fat. Mostly palmitic acid with some palmitoleic thrown in.

    The fat does not just evaporate. This is what a person's metabolism runs on during fasting. Mostly saturated fat. And fasting is excellent for plaque reversal, we're told. And I believe it.

    The question to me is, what would happen if you replaced that lost fat, by mouth, with similar fat (palmitic and palmitoleic, ie lard) to produce weight stability? Would you continue reversal without fasting? Perhaps throwing in 50g/d high quality protein to stop muscle loss.

    Obviously anyone on a low fat diet, needing to maintain weight stability, requires a high carbohydrate intake with its associated and inevitable post prandial hyper-insulinaemia. No insulin, no glucose uptake. We need calories to live. 1000kcal of lettuce needs insulin for every molecule of glucose it releases. Once a low fat vegan has lost their palmitic acid based excess weight, they'll be right back on to glucose based metabolism.

    Fasting is fat fueled. It works for reversal. Whether from your adipocytes or your plate, it's the same palmitic acid.

    Peter

  • Dr. Davis

    1/8/2008 1:39:00 PM |

    Hi, Peter-

    Interesting thoughts.

    It makes me wonder again whether there are ways to accelerate the process of plaque reversal. While we typically achieve it in a 12-18 month long timeline, could it be achieved in a less than 4 week period? Could we do so by using specific nutrient manipulations during fasting?

    I don't know, but I'm hoping that we can inch towards some insight towards this process.

  • Anonymous

    1/8/2008 3:26:00 PM |

    It's pretty strange seeing you promoting a Vegan doc...flies in the face of much of what you've been talking about.  And water-only fasts are tremendously muscle-wasting.

  • Dr. Davis

    1/8/2008 3:47:00 PM |

    I'm not promoting anybody.

    I am entertaining interesting concepts from people who provide unique or differing views.

    Coronary disease is potentially a life-threatening disease. If I need to sacrifice some recoverable muscle mass in order to substantially control or reverse it, then it's a small price to pay.

  • Peter

    1/8/2008 8:30:00 PM |

    Anonymous,

    If I could just clarify my own opinion:

    A vegan on a water fast, after the first 2 days, is living on animal fat and animal protein. Their own. They will obviously die if they continue, although possibly without arteriosclerosis (makes you think of Pritkin). Supplying that same person with 150g of lard and 9 whole eggs (biologically eggs are the highest value protein according to the WHO) per day will provide the same metabolic conditions as fasting without the fasting, weight loss or muscle loss. The question then is whether this will continue the rapid reversal of arteriosclerosis. That is open to debate, and no doubt we all will have our opinions. I invite the use of logic. I've said before, I visit here as Dr Davis is open to ideas which do not necessarily tally with his own. That's good.

    Peter

  • wccaguy

    1/9/2008 2:14:00 AM |

    Dr. Davis,

    I'm not a doctor or a scientist so what do I know?  nothing...  And I'm probably not going to restate Peter's argument very well.

    But it seems to me that in the rethinking of diet that you're engaged in, partially triggered by the Taubes book, you're going to need to address this argument that Peter makes.  I had never heard that argument before but I can't think of an escape from the logic of it, namely:

    1) during fasts, plaque regresses, 2) during fasts, body fat (which Peter says is mostly saturated fat) is used to provide energy, but 3)  how could plaque regress if a metabolism running on saturated fat was harmful to that regression process?

    It would be very interesting to hear what Dr. Fuhrman thinks about this too.

  • Dr. Davis

    1/9/2008 3:26:00 AM |

    Hi, WC--

    I don't have a pat answer for you, but I think the conversation opens up some very fascinating avenues for further thought and exploration.

    Of course, fatty acids do not just enter and exit cells passively depending on concentration gradients, but do so under the control and influence of a number of factors.

    Nonetheless, I think we are onto something, this idea of "enhanced fasting" to achieve accelerated reversal. Hmmmm....

  • chickadeenorth

    1/9/2008 5:52:00 AM |

    Just a thought, don'T know if its related or not....When people stalled out on weight loss Atkins suggested a fat FasT for 4 or so days eating macadamina nuts,olives, egg salad with whole fat mayo,even a few T OF OLIVE OIL.It seemed to reboot the metabolism...don't know about plague reversal but it stopped hunger and people started to lose again, he said not too do this until the plateau was a month long, I cant recall exact time frames.
    Its so contrary to what we have been led to beleive but if I knew it would reverse my plague I would do it, but would have to see how to balance BG, maybe have to go off glucopaghe while doing it and monitor lots.

    Several on Bernsteins site fast alot in the week to regain control of bg.

  • wccaguy

    1/9/2008 11:30:00 AM |

    I read your new special report at  Track Your Plaque that is an interview with Dr. Fuhrman on fasting and had some thoughts.

    I confess that my head is still spinning by the argument that Peter has made in his comments to this post.

    When I first read Peter's argument, it reminded me more than anything else of the first paragraph of Gary Taubes' NYT Magazine article a few years back when he described the irony that would be many doctors standing naked in Times Square moment:

    Dr. Fuhrman, an ardent vegan, promotes fasting as a helpful solution for reducing plaque without realizing and surely without understanding that the reason the solution works is because it amounts to increased animal fat consumption.

    I have to say that I'm completely unimpressed by any explanation or theory Dr. Fuhrman's put forward, either in his first book or in his interview with you, about WHY fasting works to regress plaque or at least reduce angina symptoms.

    Am I missing something and he actually can and does explain why it works?

    Peter, on the other hand, has put a theory on the table about why it works that could be tested, right?  Or has it already been tested?

    If and when the moment comes when a lot of doctors are standing naked in Times Square, I'm going to be there with a camera.  lol

    As always Dr. D, thanks for the post and for attracting some great minds who make posts that are fascinating reads.

  • Dr. Davis

    1/9/2008 1:42:00 PM |

    To my knowledge, formal clinical research on the effects of fasting (i.e., controlled "starvation") are woefully limited. I know of no studies that examine the effects of specific nutrient feeding to fasting or starving subjects. But it would be fascinating.

  • Anonymous

    1/10/2008 2:33:00 PM |

    The other aspect in common between fasting and a very low-carb diet are the ketones. It might be that the ketones are responsible for a bettering of heart condition as it is most efficient fuel we can use.

    There is a difference though between them, one is catabolic the other is anabolic, so they may not be exactly equivalent.

    Just some random thoughts.

  • Dr. Davis

    1/10/2008 4:16:00 PM |

    What an interesting idea!

  • Peter

    1/10/2008 9:15:00 PM |

    Excellent point

    Yasiwaya points out that ketosis restores the mitochiondrial function lost in insulin resistance, best quote:

    "The ability of a physiologic ratio of ketone bodies to correct most of the metabolic defects of acute insulin deficiency suggests therapeutic roles for these natural substrates during periods of impaired cardiac performance and in insulin-resistant states"

    Some of the other papers by this author, available in full text by hitting "related links" suggest a deep in depth knowledge, but they're way beyond me.

    For those of us who long ago abandoned the cholesterol hypothesis, hyperinsulinaemia and insulin resistance are the driving forces of IHD. The Yudkin/Stout camp. Ketosis appears to side step insulin resistance, be that in the myocardium or the cells of the arterial media. I would wholely agree this is a useful step in IHD and may well be where the benefits come from.

    Peter

  • Dr. Davis

    1/10/2008 10:11:00 PM |

    I have to admit that I hadn't thought of ketosis as a process with its own health consequences, just as a consequence itself. This may be worth investigating!

  • Anonymous

    1/11/2008 2:26:00 PM |

    Dr Davis,  been meaning to mention, I've been informed that the company Vassol Inc, there web sight is http://www.vassolinc.com/, has succeeded in being able to scan the "moving" heart with an MRI machine.  I was told that the company is now working with the NIH in conducting further studies.  Thought you might find interesting as I imagine an MRI would be helpful with wanting to check quick progress on patients.

  • e4e

    8/8/2008 3:57:00 AM |

    Yeah but...

    Why use BMI? Why not use body fat directly instead?

  • Bruce K

    8/12/2008 7:30:00 PM |

    Peter, I would use butter, ghee, or beef fat instead of lard (2-4% PUFA vs 12%). You're wrong that eating a high lard diet would be the same as fasting. On a fast, you don't eat a gram of PUFAs. 150g of lard has 18g of PUFAs. 150g of beef tallow has 3 to 4.5 grams, or 1/4 to 1/6 as much as lard. Ruminant animals are best. Also, eggs are unnecessary. You can eat fat from meat, butter, and some organ meats every now and then. The eggs have more than PUFAs than beef and butter fat. To really reproduce the fasting state, I would keep the PUFAs as low as possible (3-4g).

  • Anonymous

    1/31/2011 5:44:48 AM |

    Fasting induces autophagy, a process that recycles cellular structures that range in size from proteins to organelles. It's central to many processes of biological repair.

    Research in autophagy is growing very fast, and must be relevant here.

    (BTW, niacin and other antilipolytic agents also induce autophagy.)

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Vitamin D: New Miracle Drug

Vitamin D: New Miracle Drug

At the meetings of the American Society of Bone and Mineral Research, Dr. Bruce Troen of the University of Miami detailed his views on the extraordinary benefits of vitamin D replacement. He also talked about the enormous problem of unrecognized vitamin deficiency.

“There’s a huge epidemic of hypovitaminosis D, and the real key here is not just that it’ll benefit you from a bone and neuromuscular standpoint, but if you correct hypovitaminosis D and the corresponding secondary hyperparathyroidism, then you’re going to decrease prostate cancer, colon cancer—actually “up to 17 different cancers, breast cancer included.”

Unfortunately, Dr. Troen did not talk much about the heart benefits of vitamin D, likely since the data is scant, nearly non-existent. However, if the Track Your Plaque experience means anything, I predict that vitamin D replacement will become among the most powerful tools you can use to gain control over coronary plaque.

Read the text of a report from the Internal Medicine World Report to read more of Dr. Troen's comments.


http://www.imwr.com/article.php?s=IMWR/2006/11&p=40
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