Harpoon

Reducing Global Demand For Food And Fuel By Reducing Obesity

If fat people would eat less and walk more instead of driving, the world problems of high food and oil prices could be alleviated.
 

Sadly this naive conclusion is not the product of some troll on a random internet forum but is in fact the summary of correspondence published in The Lancet.

It is also argued that since the mass of the obese population is greater than a normal population, more transportation fuel energy is required to transport the obese. This is only likely to worsen since obese people will choose to walk less and drive more in response to their increased body mass.

There is little point in addressing such a proposal which is essentially the application bad medicine to a misunderstood matter of economics. The authors betray both a lack of insight into the nature of obesity as well as global market forces.

The greatest gains, they say, would not be through a general decline in car use, but through a reduction in the excess food and car use demands that come from the obese portion of the population.

Without really wanting to “go there” it might be worth pointing these people to studies which suggest that it takes far more food calories than petro-carbon calories to move a body… so the economies they are expecting might just not work out.
 

But that’s not really in the spirit of what they are saying… which is effecitvely “these people are getting more than their fair share of food and oil to haul their fat asses about. If only we could trim them down then the world is saved.”

The obese population, therefore, requires more than 18% more food energy than a normal population.

The sad part is that this kind of thinking is mainstream and it’s what many people face when they go to their doctor for advice on weight management.

Start walking and don’t eat so damn much. And by the way, your fat is making it rather expensive to run the Benz.

Please.

 
Psst. Perhaps fat people are responsible for global warming too… it’s those thighs… and all that friction.

Testing out Vodpod…

And if that doesn’t work, this is worth a look…

Just for fun…

JS would approve

Via

This story blew me away:

A female patient in her 50s, with lung cancer, came to our clinic, having been given a death sentence by her Florida oncologist.

She was cooperative and understood the connection between nutrition and cancer. She changed her diet considerably, leaving out 90 percent of the sugar she used to eat. She found that wheat bread and oat cereal now had their own wild sweetness, even without added sugar. With appropriately restrained medical therapy—including high-dose radiation targeted to tumor sites and fractionated chemotherapy, a technique that distributes the normal one large weekly chemo dose into a 60-hour infusion lasting days—a good attitude and an optimal nutrition program, she beat her terminal lung cancer.

I saw her the other day, five years later and still disease-free, probably looking better than the doctor who told her there was no hope.

Cancer’s Sweet Tooth

The Warburg Effect is not news but to hear of a case where Lung Cancer was actually treated with, in part, sugar deprivation, is brilliant.

Via radical blog extraordinaire Hyperlipid.

More research on our rodent friends who by now should have every mechanism worked out in order that they stay slim.

Blocking a particlar enzyme (CaMKK2) was shown to decreases appetite And promote weight loss.

I found this observation odd:

They also studied both normal mice and mice missing CaMKK2 to learn how these types responded to low-fat and high-fat diets. After nearly 30 weeks on the specific diets, the normal mice on the high-fat diet became diabetic — they were unable to respond to insulin and weren’t able to manage blood sugar levels well. In contrast, the normal mice on a low-fat diet stayed healthy.

In mice missing CaMKK2, the scientists found that they stayed healthy regardless of whether they were on a low-fat or high-fat diet. The CAMKK2-negative mice apparently were protected from changes that lead to diabetes in a high-fat diet.

I don’t understand how a high-fat and presumeably low-carb thus low insulin producing diet would lead to diabetes. I’m open to suggestions. I assume we don’t have all the facts.

I suppose if the carb-content of the two diets remained the same it could make sense…?

Duke Medical News

The Daily Mail has some fantastic pictures of Macaques which have grown fat on food that tourists have fed to them. Via Ugly Overload

It’s one thing when we do this to ourselves, but for the zoo to let this happened to these creatures that already suffer from captivity is IMO animal abuse.

It’s been a busy week…

New genetic variants that influence fat mass

Half the UK population has the fat “gene” - ie “sequence of genes”
…which I affectionately call the “I can’t eat this crap” gene

The sequence they discovered is not a gene, but it sits close to a gene called MC4R, which regulates energy levels in the body by influencing how much we eat and how much energy we expend or conserve. It is thought the sequence might play a role in controlling activity levels of the MC4R gene.

Dairy claims false: neither dairy nor calcium intake promotes weight loss

“Our findings demonstrate that increasing dairy product intake does not consistently result in weight or fat loss and may actually have the opposite effect,” the authors conclude.

Human metabolic phenotype diversity and its association with diet and blood pressure: Causes Of Disease Can Be Revealed By Metabolic Fingerprinting

Metabolic fingerprinting looks at the relative levels of many different metabolites, which are the products of metabolism, in a person’s blood or urine. Metabolites act as markers which can reveal a lot about how diet and lifestyle contribute to risks for certain diseases.

Aspirin-like compounds increase insulin secretion in otherwise healthy obese people

Aspirin-like compounds (salicylates) can claim another health benefit: increasing the amount of insulin produced by otherwise healthy obese people. Obesity is associated with insulin resistance, the first step toward type 2 diabetes.

How is that a benefit? Useful info but bad analysis. Good deconstruction here.

I missed this one earlier… Ha! I didn’t see it until it hit the BBC….
Vitamin A, E & Beta-carotene “seem to increase mortality”
I’d love to hear what the stats were on Vitamin D but it wasn’t covered

After various factors were taken into account and a further 20 studies excluded, the researchers linked vitamin A supplements to a 16% increased risk of dying, beta-carotene to a 7% increased risk and vitamin E to a 4% increased risk.

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If you haven’t already done so, be sure to read The Vitamin D Newsletter reprinted over at The Heart Scan Blog.

Some highlights.

Lack of vitamin D correlated with numerous cancers

Dr. William Grant reported that 15 cancers (colon, esophageal, gallbladder, gastric, pancreatic, rectal, small intestinal, bladder, kidney, prostate, breast, endometrial, ovarian, Hodgkin’s lymphoma, and non-Hodgkin’s lymphoma) are associated with lower UVB light. He concluded that 257,000 cancer deaths in 2007 in the USA were accounted for by inadequate vitamin D levels.

Professor Robert Heaney and Joanne Lappe’s randomized controlled trial [showed] that increasing baseline levels from 29 to 38 ng/ml reduced the risk of getting cancer by around 70%.

Type-1 Diabetes correlated to latitude and UV light

Cedric Garland began by showing the incidence of type-1 diabetes and multiple sclerosis by latitude. I had no idea that the latitudinal data was so strong for type 1 diabetes in children. This disease is almost nonexistent around the equator.

Ideally we need blood 25(OH)D levels of about 50 ng/ml

Hollis and Binkley’s crucial discovery was that the body doesn’t start storing the parent compound, cholecalciferol, until 25(OH)D levels reach about 50 ng/ml. They showed, using basic steroid pharmacology, that 50 ng/ml should be considered the lower limit of adequate 25(OH)D levels.

D is key in DNA

[Robert Heaney] covered calcium absorption, osteoporosis, risk of falling, muscle function, death and disability of the aged, TB, influenza, cardiovascular disease, hypertension, diabetes, cancer, multiple sclerosis, and gum disease. How can one vitamin be involved in so many diseases? Simple said Dr. Heaney, “vitamin D is the key that unlocks the DNA library.”

In modern times, pregnant women need high levels of supplementation to maintain healthy levels for herself and her baby

… when pregnant women keep their levels where we think prehistoric human levels were, about 50 ng/ml, breast milk becomes a rich source of vitamin D. First [doctors Carol Wagner and Bruce Hollis] gave 2,000 IU per day, then 4,000 IU per day and finally 6400 IU of D3 per day to lactating women. Only at 6400 of D3/day did the women maintain both their own 25(OH)D levels and the levels of their breast feeding babies above 50 ng/ml. On 6400 IU/day, the vitamin D activity of the breast milk went from about 80 to 800 IU/L. Quite a discovery, and another reason for all of us to keep our levels above 50 ng/ml.

Most of us could use about 2000 IU per day, but some of us need more…

Then Professor Heaney addressed a public health question. How much would we have to give all Americans to get 98% of people above 32 ng/ml without causing toxicity in anybody? The answer: 2,000 IU per day. Of course 32 ng/ml is not adequate but it would be a great first step. Furthermore, of the people left out, a high percentage would be African Americans. In fact, Dr. Talwar recently reported that 40% of African American women fail to achieve a level of 30 ng/ml even after taking 2,000 IU/day for a year.

Note: Natural sources of Vitamin D include many cold water oily fish.

The easiest way to get your vitamin D is to follow grandma’s advice: take Cod Liver Oil.

Yes I learned to cook because of Youtube. And years of experimentation which often didn’t end well.

How To Peel an Egg

Perfected Tradition

Speed Peel

Egg Education

• How to cook the perfect hard-boiled eggs
  156 Fareheit for 4 hours. No kidding.
• Microwaved thin egg sheets (usuyaki tamago)
• Are Eggs Nature’s Statin?
• Hard boiled eggs in a bag. Sadly true.

The Perfect Scrambled Eggs

The Perfect Poached Egg
I seem incapable of poaching an egg but I keep trying…
Gordon Ramsey also has a useful video on this topic which demonstrates the swirling technique… this gives a slightly different shaped result.

Deviled Eggs
OK look - if you didn’t know how to make these you could probably figure it out without a video. But this woman has such a long lost June Cleaverness to her that it’s worth watching.

For a quicker video, check out Cooking for Men (which incidentally includes tobasco which has a certain machismo to it).

You know times are changing when people like these bring video cameras into their kitchens and start posting on YouTube.

There’s some fresh research out substantiating the theory that fat cell numbers are set by the end of adolescence and remain stable in adulthood, regardless of weight loss. Fat size can vary but cell numbers remain constant.
 

The research has also shown that each year, approximately 8% of fat cells die off and are replaced. As such, cell numbers are maintained.

So no news here.
 

But what I’d be interest to know, is whether liposuction would be successful in effecting a long term reduction in the number of fat cells or if, over time, cells removed are repopulated.

In other words, does the body
(a) work towards maintaining a certain number of fat cells that is set in adolescence, or
(b) simply have a tendency to replace a given number of cells each year and thus surgery is a viable long-term method to reduce fat cell numbers?

If surgery truly reduces fat cell numbers for good, then liposuction could effect a permanent change in a person’s fat distribution pattern. If it cannot, then the results will only be temporary and that pear shape will eventually return.

I suspect that (a) is true and that, suck up what cells you might, eventually they will be repopulated.

This suspicion is based on some research I vaguely recall in which obese mice had some fat removed from their bodies and then immediately increased their food consumption to compensate until the fat mass was restored.

Of course the increase could have been effected by the enlargement of the residual cells. But given that our genetics program us to deposit fat in specific places (varying slightly from individual to individual), it would seem that taking a vacuum to your big butt would have no impact on your general tendency to put fat in that area.

Saying that, I’m not familiar with the long term results of liposuction so I may just be talking out of my own big butt.