He did practice a vegetarian, whole-grain focused diet. I believe he was influenced by Ghandi. I have read articles by the grand daughter which do not promote a diet exclusive of meat, though, so times have changed. He farmed organically with no source for manure or bone meal - I always wondered how depleted the farm's soil was. Rodale publishing heavily propmotes exercise through its Prevention walking teams, and by publishin Running Times, Runner's World and Men's Health. Men's Health has the best low carb editing anywhere.

I read Men's Health and get their e-newsletters! They are not low-carb. They have an Abs Diet they promote separately in books and magazine supplements but they don't shy away from healthy burgers with buns, fruit, a healthy pizza, etc. Prepared foods are plentiful in their 'Eat this, not that' series.

Neither is Prevention low-carb, for that matter. However, whatever Rodale's personal preferences, his magazine has not been vegetarian. And whatever his methods of organic gardening, his magazine 'Organic Gardening' (which I haven't seen in a long time so I don't know if it's still produced by Rodale) is a classic source for organic gardeners.

When I worked for a defense contracting company, the land around our complex was large and open (few trees) so we had organic gardens. The library in the complex stocked 'Organic Gardening' just for us. There were some who didn't want to go organic, and their gardens were distanced from our area. I don't remember there being anything radical about Rodale's gardening methods, not from that magazine.

Prevention Magazine promotes walking a LOT. However, there are always articles about lifting and resistance training in Prevention. They tend to keep exercise pretty simple and I, myself, don't really like it when they picture people doing things in the gym that require machines. I belong to the Y and work out there (not much lately) and I do use machines. But I think it can put some people off to think that exercise is going to involve joining a gym or using machines.

Also, Prevention does promote hiking, swimming, anything that makes you move your body! And they make it sound like fun, relaxing and stress-reducing. It's a whole different vibe from Men's Health, in that sense.

Dr. Atkins had cardiomyopathy - which was reported by his physician to be caused by a viral infection, and not related to his diet.

Just wanted to point that out.

I think it's harder to get obese that you think Try reading this article about getting fat in prison.


PS
If when cutting and pasting from other posts you enclosed that excerpt with [quote ] without the space then [/quote] I would find it much easier to read your posts. If you are posting regularly you will find your fingers type those codes so fast you won't find it slows your posting down at all.

Okay, according to Bob, exercise is behind most of the weight loss on the Biggest Loser. To a man with a hammer, everything looks like a nail.

I wonder if the show's nutritionist thinks it's all about the diet? I do think that heavy manual labour, coupled with a controlled diet, will usually lead to weight loss. But that presupposes that a person is capable of heavy manual labour, and of a controlled diet while doing all that work.

One big weakness of the Biggest Loser as a weightloss study is that those who don't thrive on the program tend to get kicked off. On a recent show, Bob complained that in the last season finale, a lot of people showed up having made no real progress in their weight loss since being sent home. I've seen a personal trainer online say that their program is 100 percent effective for those who stick with it. But who sticks with it? Those with stronger willpower? Or those who can? (The "challenges" on TBL certainly help to weed out the less physically capable contestants.)

I also think that bed rest isn't just about exercise, whether it's in a hospital bed or at home, it's a changed environment. Since most people don't eat most of their food in their bedrooms, certain sights and smells that trigger appetite might be missing.

I have seen episodes of the Biggest Loser where exercise didn't seem to match weight loss. Where someone was injured and won the weigh-in for the week. Or where some of the contestants were outnumbered by their rivals, so they snuck out early and put in hours and hours of extra exercise, only to lose the weigh-in.

Rodale started organic gardening in the 40's - Prevention magazine came later, maybe in the 60's? The magazines have never been just a mouthpiece for his ideas. Men's Health does not offer just low-carb advice, but they will run stories about saturated fat being OK, for example, and teach you the best ways to make fatty steaks. It's a mixed bag and there are a few different editors involved, but one of them is very pro low carb (I cannot remember his name).

True!

http://lowcarbdiets.about.com/gi/o....diet/index.html


But thanks for sending me searching through google for more information. The 'smoking gun' website has the death certificate with notes from the medical examiner. I'm suspicious - but I think the medical examiner has ample opportunity to clear up those notes he wrote on the death certificiate about 'hypertension, myocardial infarction and congestive heart failure.' If I were the family, or Atkins' doctor, I'd sue if those are falsehoods. They should.


Atkins' widow stated, after the medical examiner's report was released:

'While Robert did have some progression of his coronary artery disease in the last three years of his life including some new blockage of a secondary artery that was remedied during this admission, he did not have a heart attack.'

He died from a fall, people! All the hoopla after his death was quite mean-spirited. But he did have 'progression of his coronary artery disease' according to his widow, the M.E.'s report was leaked, and the man was just like any other guy who was 72 years old - age brings risk from which, I don't think, in his case, Atkins was afforded any special protection. He wasn't in perfect condition, despite his diet. His heart health in the past hadn't been perfect, despite his diet. In that respect, was he any different from Rodale? I don't think so.

RIP, Atkins.

And the more I dug around, the more surprised I was by what I found.

I didn't know, for example, that Gary Taubes is in on this thing called 'Innovative Metabolic Solutions.' Thank you, Jimmy Moore!

http://livinlavidalowcarb.com/blog/...alth-risks/8686

https://www.myimsonline.com/

How did I not know about Taubes doing this thing?

'I've seen a personal trainer online say that their program is 100 percent effective for those who stick with it. But who sticks with it?'

Teaser, I think that is the story behind the success of ANY regimen. Personal trainers probably know that better than anyone!

http://www.ncbi.nlm.nih.gov/pubmed/19633334

For men, in particular, it's more difficult and takes longer to become obese (due to hormones, I think). But the prevalence of obesity in prison involves the same issues, and the same obstacles, except physical activity is curtailed. It is allowed in a 'window of opportunity' for sports and jobs in prison don't necessarily involve much physical activity.

http://www.ncbi.nlm.nih.gov/pubmed/3984358

addresses women's weight gain in prison.

And is it any surprise that, when your food is a prison diet, and you are lucky if you get food 'from the outside,' you are at the mercy of the institutional food budget? Should these women have their diets examined because, it turns out, their cholesterol levels were lower than women outside prison?

http://www.ncbi.nlm.nih.gov/pubmed/17572105

Either I'm doing some really crappy searches or NCBI offers really very little data about how people gain weight in prison. Surprising, since they truly are a captive population for study.

The Gina Kolata article about gaining weight was interesting. But I found it much more interesting to look at an original study by Sims. It was an article about adipose tissue. I don't know if it is the particular study she cited but it was about lean men getting fat in prison.

What's easiest for me is just to use quotes. And cutting and pasting from a PDF is awkward, but I do it anyway... sorry, that's the way I do it.

Sims wrote:

'These observations in experimentally
induced obesity lend further credence to the concept
that adipose cell number may be altered only early
in life, and provide additional evidence for believing
that human obesity may be categorized according
to the cellular pattern of the adipose depot: early onset
obesity characterized by a hypercellular adipose mass and
adult onset a normocellular, hypertrophic tissue.
These conclusions should, however, be drawn with
great care, as the following considerations sugggest.
The changes in the current study were experimentally
and acutely induced, and the degree of obesity which resulted
was relatively mild. In spontaneous, lifelong human
obesity the abnormality is a more chronic one and
is usually more severe. It is possible that years of excessive
caloric intake in adult man leading to severe expansion
of the adipose depot could lead to changes in cell
number. Bray and Gallagher have reported a marked increase
in adipose cell number in an individual who became
obese as an adult as a result of a hypothalamic tumore
. Although Hirsch and Knittle report that
increased cell number is characteristic of the adipose depots
of patients with early onset obesity, there is some
increase in cell number in individuals whose obesity began
after age 20 . Thus, the question of when and,
if cell number becomes fixed remains unsettled. Additionally,
the current data indicate that there may be significant
differences in the size of adipose cells from one
subcutaneous site to another in nonobese individuals. In
this respect, the data differ from those of Hirsch and
Knittle but are consistent with the recent observations
of Goldrick and McLaughlin. The significance of
these findings lies in the fact that total adipose cell number
of the body is calculated on the basis of mean fat cell
size. Thus, until the size of adipose cells in all major fat
depots of the body as well as the relative contribution of
each depot to the total adipose tissue mass can be defined,
conclusions about differences in total adipose cell
number between individuals when calculated on the basis
of one, two, or even three subcutaneous sites should be
drawn with caution. This is particularly true in view of
the observation that in some individuals omental and
mesenteric fat cell size may differ considerably from
those in the subcutaneous depots.' The possibility that
intra-abdominal and subcutaneous fat depots are influenced
differently in obesity (spontaneous or experimentally
induced) has not been excluded by these studies.
An additional factor must be considered in interpreting
the present data as well as those of Hirsch: the sensitivity
of the method used for cell counting to detect very
small fat cells. It should be noted that according to
Hirsch and Knittle , in a few obese subjects who had
undergone extreme degrees of weight loss there was an
apparent reduction in total adipose cell number. The authors
believe this apparent reduction in cell number to
be artifactual since the method used for cell counting
depends on the lipid content per cell. Thus, cells containing
less than 0.01 /Ag of lipid might not be counted,
leading to an erroneous overestimation of mean cell size
and underestimation of total cell number. The apparent
reduction in cell number was found only in those individuals
with extremely small cells. Similarly, it is possible
that precursors of adipose cells containing little
lipid may exist in the adipose depot and thus not be measured
by the present techniques . If forced feeding
induced the formation of substantial numbers of these
precursor cells, an increase in cell number would go undetected.
Thus, although the current data taken together
with those of Hirsch and coworkers seem to support the
concept of a fixed number of adipose cells determined
early in life and the categorization of obesity into two
cellular types, for the above reasons some modification
may be necessary.
In spite of site-to-site variability in adipose cell size
the current data indicate that in these individuals the
lipid content per cell increased relatively uniformly over
the three sites examined. This is contrary to the gross
impression of earlier studies in experimentally induced
human obesity in which it appeared that the excess subcutaneous
fat was preferentially deposited in central
rather than peripheral depots . Such differences may
reflect differences in the total number of fat cells in a
given subcutaneous depot.
The data in the current study do not indicate that those
subjects who were fatter initially and who gained more
weight (A. C., N. H., B. H.) had either more cells or a
tendency towards a change in cell number when compared
to their leaner colleagues (R. P., P. W., S. L.,
L. M.).
The mean values for adipose cell size in the seven patients
of this study are below those reported by Hirsch
and Knittle using the same technique . One possible
explanation may lie in differences in body weight between
the two groups: individuals in the current study
weighing less. Hirsch and Knittle do not provide information
on the body weights of their nonobese group.
Other differences in technical procedures between the
two laboratories may play a role in these differences.
The present studies indicate that experimentally induced
obesity in adult humans is achieved primarily by
an increase in adipose cell size without a change in adipose
cell number. It is well recognized that weight gain
and increased adiposity under these conditions are associated
with the development of abnormalities of carbohydrate
and lipid metabolism. The mechanism(s) by
which this occurs is unknown. Studies currently in progress
in these laboratories are examining the role of factors
such as dietary intake and physical activity as well
as adipose cell size and insulin sensitivity in the development
of these metabolic abnormalities of obesity.'

My bold - I think that was the point of his study.

This was
'Experimental Obesity in Man: Cellular
Character of the Adipose Tissue
LESTER B. SALANS, EDWARD S. HORTON, and ETHAN A. H. SIMS
From the Department of Medicine, Dartmouth Hitchcock Medical Center,
Hanover, New Hampshire 03755, and the University of Vermont Medical
School, Burlington, Vermont 05041'

It appeared in 1968. Accessible from NCBI.

http://www.ncbi.nlm.nih.gov/pubmed/5721398

I don't agree with all that Gina Kolata thinks is implied by the studies, or even what the various researchers concluded. It does seem to me that size and number of adipose cells make a difference. Can you increase the number of adipose cells and then be stuck with dealing with that number (that can increase in size, each of them!) and how do you do that?

I'd have to spend more time reading the Kolata article and yet I already know that there are studies about adipose cell number. I'm just not going to delve into those waters right now!

Why then can I maintain my weight loss without exercise, without calorie restriction or counting and without carb counting only restricting those refined carbs that that raise insulin high and fast?

You need to understand the secret is to ignore calories in and calories out and concentrate on why your appetite is calling for food and the reasons underlying a lack of energy.

Dealing with the cause of the problem rather than treating the symptoms means that there is NO EFFORT involved and therefore "Sticking with it" isn't an issue.

Inflammation is the root cause of the problem.
That determines the type of gut flora that thrive in your digestive system.

An inflammatory diet/lifesyle/environment means obese type gut flora that extract the maximum calories from food consumed will dominate.
Dealing with excess inflammation by correcting omega 3 imbalance and correcting vitamin d3, magnesium deficiency states permits lean type bifidobacteria and other lean type gut flora (that are not so efficient at calorie recovery) to dominate and so you have a lower appetite, less likely to overeat, find it easier not to snack between meals. Swapping from pro inflammatory omega 6 oils to coconut oil promotes ketone burning and this also improves energy levels and reduces appetite.

By continuing to focus on the symptoms of obesity rather than the causes you perpetuate the problem and increase the chance of people not sticking with it.

If you deal with the causes of overeating and lethargy, use ketone burning and Intermittent fasting to encourage mitochondrial biogenesis to replace dysfunctional mitochondria while changing obesogenic pro inflammatory gut flora to anti inflammatory lean type gut flora you solve the underlying cause of the problem and set the scene for successful weight loss and sustained weight maintenance.

Metabolic Syndrome and Altered Gut Microbiota the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.

Using effective amounts of vitamin D3, omega 3 magnesium and zinc together with curcumin will improve immune function and reduce inflammation in the digestive system. Both vitamin d and curcumin inhibit pathogenic gut flora and the omega 3 promotes bifidobacteria populations which in turn enable a greater conversion of ALA to EPA/DHA. (sets up a spiral of increasing omega 3 levels)

'That is why you need to understand the secret is to ignore calories in and calories out'

Sorry, that's the way I do it. I like it. It's my nature. And for all the various diets people use on this board, it's not that whacky.

She's been asked this several times. She won't do it. I find it easier to skip her posts, they give me a headache.

Skip away, Angeline.

Here's another study by Sims, possibly one that was used by Gina Kolata:

http://www.ncbi.nlm.nih.gov/pubmed/4881681

The original study is downloadable to PDF from NCBI.

Well, yes, I agree there. At least, I agree that sticking to a program will be associated with success on the program. But, did they succeed because they stuck to the program, or did they stick to the program because it was effective for them? It might be a virtuous circle, where success encourages them to stick to the program. But if sticking to the program was totally ineffective for them, the likeliness of them sticking to the program goes down. Success is pleasant and addictive.

I appreciate that for Mathmaniac and the continuous diet function it is your lifestyle choice to be permanently on a diet but for lesser mortals who are unable to stick with a continuous diet mentality it is a whacky idea.

Naturally humans should be able to eat the food that is available and stop when the appetite is satisfied and to exercise only as much as is required.

If you need to be continually concerned about counting calories in and calories out rather than correcting the natural metabolic regulating systems so these matters are dealt with subconsciously then you are failing your system and creating a climate where ultimately failure is inevitable.