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!

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

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.

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.

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.

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

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.

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....

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.

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.

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.

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.

What an interesting idea!

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

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!

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.

Yeah but...

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

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).

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.)

Some thoughts I have about the causality vs. correlation. Those studies that show correlation with increased mortality /disease with sleep times longer than 9 hours per day could suggest that people with deseases sleep longer because of the disease?  Not that longer sleep periods them selfs are the cause of the disease and early death but a sign of troubles in health which need more time for the body to trying to recuperate?

I personally sleep between  7 - 9 hour per day if I can rest up to my taste, but if I'm stressed I sleep less and if I'm sick I sleep more.

(Sorry for possible spelling mistakes, I'm not native english speaker.)

WBR:
JVAS

Anon--

Excellent point.

In fact, I wonder if greater sleep need is, for many, a red flag for hypothyroidism, in addition to other conditions.

Brain study shows differences in night owls, early risers
Last Updated: Tuesday, June 23, 2009 | 5:36 PM MT  
CBC News  

Scientists at the University of Alberta have found there are significant differences in the way our brains function, depending on whether we are early risers or night owls.

Using magnetic resonance imaging-guided brain stimulation, neuroscientists tested muscle torque and the excitability of pathways through the spinal cord and brain.

"We found that the brains of morning people are more excitable in the morning and evening people are completely opposite," neurophysiology researcher David Collins said Tuesday.

"The evening people ... it's almost a perfect storm of excitability in the central nervous system, where the brain is maximal in the evening and the spinal cord is maximal in the evening.... They generate the most force in the evenings," he said.

David Collins, neurophysiology researcher at the University of Alberta (CBC) "Morning people ... their brains are most excitable in the morning, but their spinal cords are most excitable in the evening," Collins said.  

The results may suggest that morning people are performing below their maximum possible level at all times of the day because of this, he said.
Morning person may be steadier

If you could change morning people into evening people, maybe their performance would be best in the evening, he suggested. This doesn't mean it's necessarily better to be an evening person, he said.

"A morning person may be a more consistent, steady plodder over the course of the day," Collins said.

Kaitlin Cleveley, a sports performance researcher at the U of A, likes to begin work around 10 p.m. and go until 3 a.m.

"Anything that starts in the morning is absolutely brutal for me to try and get up and try and function," she said. This study brings new perspective to training, she said.

"It's about trying to peak the athlete.... It can help to set up a sleep program, and it can help to reduce jet lag and sort of help you to determine you know 'When should I book the flight?, When should I get there?'" Cleveley said.

The research has lots of applications, including understanding mental and physical peaks and how people can maximize performance, she said.

Initially the research was to determine if brain function changes over the day, Collins said.

The study evolved with some early findings around two subjects in the study. One proved to be an extreme morning person, the other an extreme evening person, he said.

How does napping fit into this?  Does napping count in the "hours per night" or is it separate?  Any statistics on mortality and napping?

A lot of cultures have an afternoon siesta but Americans tend to frown on napping.

A close family member just underwent double bypass surgery in the past few weeks (doing well now, though it took a blood transfusion to get over a 2 day slump while in the hospital), after more than a year of symptoms with exertion,  poor stress test results, a lot of career stress recently, etc.  None of us were told though until just before the recent angiogram.   I always viewed this situation as a "when", not an "if", because I had a different view than the AHA's, but it's always "too soon", even if expected.

The angiogram revealed multiple sites of stenosis in locations not suitable for stents, so double bypass was performed.

Aside from family history (her father died of CVD at age 50), there were other risk factors, so she faithfully followed most of the AHA guidelines since at least the 80s - regular chol panels (high results), statins, HRT, low fat/high chol, reduced saturated fat, reduced fat dairy, lean meats, lots o' carbs (even lots of whole grains), etc.  

But obviously, this didn't work (I think it's a recipe for a bypass), because  CVD happened anyway despite all this adherence to  "prevention" (I use that word loosely in this context).  

Other risk factors include tendency toward "apple" shape, "strong explosive" personality (sort of Type A), and as I suspected, diabetes (though that was concealed from the family until just before the surgery).  On top of that ...(drum roll)...

and pertinent to this post - 25+ years of working the third shift as a nurse in L & D.  She was *chronically* and noticeably sleep-deficient (very often apparent, even over the phone), not to mention also Vitamin D deficient (her calcium supplement only added a tiny amount).  The coronary calcium scan wasn't done until last year, when there was marked plaque and shortness of breath & fatigue symptoms.  Of course no program such as Track Your Plaque was suggested or undertaken.  It was fate, right? - the family history - nothing could be done to override that, right? Note: if you are reading this with a sarcastic tone, that's about right .

Talk about an AHA failure to prevent. Everything I've  I shared about about the AHA's misguided approach to prevention, low carb and grain restriction to manage BG and diabetes, and all the other ways to prevent CVD fell on deaf ears.  Still does.  Still keeping my fingers crossed that the bypass arteries don't clog up.