Comments on: a fix for both obesity and malnutrition?

By: Jon

Jon — Thu, 30 Sep 2010 00:50:36 +0000

Makes sense, obese people are not healthy eaters. People get fat as a result of sugar addiction, and sugar has no nutritional benefit, just pure energy.

Of course, rather than use the drug to combat fat, you could eat the foods in which the chemical appears naturally.

By: Lorqess

Lorqess — Tue, 31 Aug 2010 16:55:47 +0000

Sounds very interesting, perhaps the next generation of weight loss medication will be based on such research, but I still think we will be years away from a complete side effects free method, but I do think we are getting there.

By: mili

mili — Thu, 08 Apr 2010 06:12:49 +0000

How To Combine diet pills With Your Health Routine
To avoid any sort of side effect you must combine your diet pills intake with a healthy diet and routine exercising. Doing the trio of actions – diet pill consumption, healthful eating and regular activity – will yield you the best and safest results. In terms of your diet, you must eat well, and in substantial amounts as to promote definite weight loss. And note, to please, not starve yourself – this will not help you to lose weight in the slightest bit. And as far as exercise goes you should, in the least, workout 3-5 times a week to keep metabolism levels racing and your body tuned for energy utilization and overall weight loss。

By: dohfiddle

dohfiddle — Mon, 14 Jul 2008 23:29:54 +0000

The food manufacturers and processors need to be more accountable for what they actually do with our food

By: isabella mori

isabella mori — Sun, 02 Mar 2008 17:46:03 +0000

thanks for the comment, harold.

you have a good point there. i often wonder, when we are given the nutritional contents of foods, how are they measured? i have a hard time believing that a canned pea, a pea that was harvested 4 weeks ago from a heavily fertilized soil, and a pea taken off the vine from an organic garden have exactly the same nutritional content.

By: Harold Mounce

Harold Mounce — Sun, 02 Mar 2008 15:18:37 +0000

You right on about obeseity and malnutrition. Our food supply is highly suspect in being as nutritious as it once was. Food producers looking to the bottom line are wearing out the soil. They do not rotate or let land rest. Thank you for your good work…keep it up.

By: A Link Between Obesity and Malnutrition « Migrations

A Link Between Obesity and Malnutrition « Migrations — Fri, 03 Aug 2007 16:53:54 +0000

[...] Feb 20th, 2007 by Dan For an interesting post on the role of leucine (an essential amino acid) in metabolism, check out Isabella Mori’s Change Therapy. In particular, researchers at Penn State have uncovered a molecular switch that responds to changing levels of leucine in the diet, and may be involved in shifting metabolic responses. Isabella notes that this research is relevant to not just obesity, but also malnutrition and the starvation response – and so the protein, GCN2 eIF2alpha kinase, may be a potential drug target – but there are caveats as well. [...]

By: Keith Robison

Keith Robison — Tue, 20 Feb 2007 06:07:12 +0000

One other thought: even if a drug was waiting in the wings for this indication, trials in metabolic disorders are going to be very large sets of participants over many years. Since obesity is a chronic disease affecting a very broad population, the safety bar is going to be very high (previous fiascos such as fen/phen also contribute to this).
So any approved indication (i.e. it’s on the label, high likelihood of insurance reimbursement, etc) is a long way off — if there was a drug already approved or near approval for another indication. A ballpark estimate is that for a from-scratch drug this target _might_ yield an obesity drug in a decade-and-a-half but more likely two decades — since it will probably be 7-10 years of trials to prove the thing is safe (throwing in some trial misfires & delays and such). A more avid watcher of clinical trials could probably give a better estimate, but in general it suggests don’t hold your breath.

By: isabella mori

isabella mori — Tue, 20 Feb 2007 05:11:10 +0000

thank you for your comments, daniel and keith.

and thanks for making it abundantly clear that this research does not mean there will be an obesity drug in the next three months!

i think it’s very important that the general public become more savvy in understanding science. for example, it was interesting to read that working on cell metabolism is costly.

also, “gene deletion mice” – that’s not a phrase that generally runs in my vocabulary (or that of my readers, if i’m not mistaken). of course it makes sense that mice who do not have this gene at all are different from mice (or humans, for that matter!) for whom leucine is simply inactive.

and what’s mTOR? mTOR regulates translation and cell division. it belongs to a protein complex that is used by cells to sense nutrients in the environment. nutrient availability influences mTOR so that when cells are not able to grow to normal size they will not undergo cell division. (at least that’s what i gathered from google definition).

all this leads me to confirm my belief that the equation of “calories in, calories out” which claims that weight is solely dependent on how many calories we ingest is a ridiculous oversimplification. the human body is an immensely complex interplay of chemicals, and simplistic formulae like that just won’t do.

By: Keith Robison

Keith Robison — Tue, 20 Feb 2007 03:00:38 +0000

Thank you for inviting me to comment. My first response is to agree with the above poster that this work represents the initial validation of a new drug target for metabolic research. There are some important caveats to even that statement (based on reading the abstract; Cell Metabolism is pricey). In particular, they have completely ablated the gene from the mice from the get go. It is possible that GAK deficiency early in life sets up the condition they observe, but eliminating its function solely in adult mice would not do so. I suspect they have good reasons, based on other work, to suspect this is not the case, but it would appear it was not ruled out. Furthermore, gene deletion mice eliminate the protein altogether, whereas drug treatment leaves the protein in place but inactivates it. This can again make a big difference, as an inactive protein can still tie up important partners. Target validation is a very early step in the process, so it is unlikely that this will lead to anything soon. However, there are both public efforts (The Broad Institutes' Connectivity Map being the best known) and private companies trying to identify late stage or even marketed drugs which can recapitulate the effects seen in studies such as this. So there is an outside chance that something will be turned up which can be moved into the clinic quickly. One other thought: leucine deprivation is also relevant to the mTOR signalling axis, which is another key metabolic regulation circuit. A quick PubMed search suggests that links between the two pathways have been touched upon in yeast, but it didn't look well explored in mammals.