A memory of China – neuropsychiatric consultations at Songjiang Hospital/ Jiao-Tong University in Shanghai 2010

In 2010, I was privileged to be invited to participate as a visiting consultant in a full-day medical consultation at Songjiang Hospital, a beautiful, modern university medical center affiliated with Jiao-Tong University and First People’s Hospital in Shanghai.
The story was published in the local newspaper.

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Scourge of depression sees rising number of suicides, report Cang Wei and Song Wenwei in Nanjing.

Staggering base rate…

Dark days of despair drive many to the final option
Updated: 2013-02-27 09:20
By Cang Wei and Song Wenwei in Nanjing/China Daily

Scourge of depression sees rising number of suicides, report Cang Wei and Song Wenwei in Nanjing. Every three minutes, a person suffering from depression commits suicide in China and a further 11 people attempt to take their own lives.Every year in China, 287,000 people end their lives by suicide, while another 2 million contemplate the act, 70 percent of them because of depression.

via Dark days of despair drive many to the final option[1]|chinadaily.com.cn.

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How the FDA forgot the evidence: the case of donepezil 23 mg | BMJ

Not So Stories

How the FDA forgot the evidence: the case of donepezil 23 mg

BMJ 2012; 344 doi: http://dx.doi.org.ezproxy.cul.columbia.edu/10.1136/bmj.e1086 (Published 22 March 2012)

Cite this as: BMJ 2012;344:e1086
  1. Lisa M Schwartz, professor12,
  2. Steven Woloshin, professor12

Author Affiliations

  1. Steven.Woloshin@dartmouth.edu

In the first of a new occasional series highlighting the exaggerations, distortions, and selective reporting that make some news stories, advertising, and medical journal articles “not so,” Lisa M Schwartz and Steven Woloshin challenge the claims made for the new 23 mg dose of donepezil

What is the difference between 20 and 23? If you said three, you are off by millions—of dollars in sales, that is—at least from the perspective of Eisai, the manufacturer of donepezil (marketed as Aricept by Pfizer).

A little context helps make the maths clearer. Donepezil, the biggest player in the lucrative market for Alzheimer’s disease treatments, was a blockbuster, with over $2bn in annual sales in the United States alone. But the drug, first approved in 1996, had reached the end of the road: the patent expired in November 2010. Investors call this “going over the cliff,” an anxious reference to plummeting sales as market share is lost to generic competitors. Necessity, however, is the mother of invention. Just four months before the expiry of the patent, the US Food and Drug Administration (FDA) approved a new dose for moderate to severe Alzheimer’s disease: donepezil 23 mg. Is 23 an odd number? Not really, when you consider that you cannot get to 23 mg using the 5 mg and 10 mg doses that were going generic. The “new” 23 mg product would be patent protected for three more years.

via How the FDA forgot the evidence: the case of donepezil 23 mg | BMJ.

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The nervous system and metabolic dysregulation: emerging evidence converges on ketogenic diet therapy.

Front Neurosci. 2012;6:33. doi: 10.3389/fnins.2012.00033. Epub 2012 Mar 26.

The nervous system and metabolic dysregulation: emerging evidence converges on ketogenic diet therapy.

Ruskin DN, Masino SA.

Source

Neuroscience Program, Department of Psychology, Trinity College Hartford, CT, USA.

Abstract

A link between metabolism and brain function is clear. Since ancient times, epileptic seizures were noted as treatable with fasting, and historical observations of the therapeutic benefits of fasting on epilepsy were confirmed nearly 100 years ago. Shortly thereafter a high fat, low-carbohydrate ketogenic diet (KD) debuted as a therapy to reduce seizures. This strict regimen could mimic the metabolic effects of fasting while allowing adequate caloric intake for ongoing energy demands. Today, KD therapy, which forces predominantly ketone-based rather than glucose-based metabolism, is now well-established as highly successful in reducing seizures. Cellular metabolic dysfunction in the nervous system has been recognized as existing side-by-side with nervous system disorders – although often with much less obvious cause-and-effect as the relationship between fasting and seizures. Rekindled interest in metabolic and dietary therapies for brain disorders complements new insight into their mechanisms and broader implications. Here we describe the emerging relationship between a KD and adenosine as a way to reset brain metabolism and neuronal activity and disrupt a cycle of dysfunction. We also provide an overview of the effects of a KD on cognition and recent data on the effects of a KD on pain, and explore the relative time course quantified among hallmark metabolic changes, altered neuron function and altered animal behavior assessed after diet administration. We predict continued applications of metabolic therapies in treating dysfunction including and beyond the nervous system.

PMID:

22470316

[PubMed]

Posted in Complementary - Alternative Medicine, dietary, Events, Fifth Avenue Concierge Medicine, Health, keto, metabolic, new treatments, News, Psychiatry/Neurology | Tagged , , |

Reduced pain and inflammation in juvenile and adult rats fed a ketogenic diet.

PLoS One. 2009 Dec 23;4(12):e8349. doi: 10.1371/journal.pone.0008349.

Reduced pain and inflammation in juvenile and adult rats fed a ketogenic diet.

Ruskin DN, Kawamura M, Masino SA.

Source

Department of Psychology and Neuroscience Program, Trinity College, Hartford, Connecticut, United States of America.

Abstract

The ketogenic diet is a high-fat, low-carbohydrate regimen that forces ketone-based rather than glucose-based cellular metabolism. Clinically, maintenance on a ketogenic diet has been proven effective in treating pediatric epilepsy and type II diabetes, and recent basic research provides evidence that ketogenic strategies offer promise in reducing brain injury. Cellular mechanisms hypothesized to be mobilized by ketone metabolism and underlying the success of ketogenic diet therapy, such as reduced reactive oxygen species and increased central adenosine, suggest that the ketolytic metabolism induced by the diet could reduce pain and inflammation. To test the effects of a ketone-based metabolism on pain and inflammation directly, we fed juvenile and adult rats a control diet (standard rodent chow) or ketogenic diet (79% fat) ad libitum for 3-4 weeks. We then quantified hindpaw thermal nociception as a pain measure and complete Freund’s adjuvant-induced local hindpaw swelling and plasma extravasation (fluid movement from the vasculature) as inflammation measures. Independent of age, maintenance on a ketogenic diet reduced the peripheral inflammatory response significantly as measured by paw swelling and plasma extravasation. The ketogenic diet also induced significant thermal hypoalgesia independent of age, shown by increased hindpaw withdrawal latency in the hotplate nociception test. Anti-inflammatory and hypoalgesic diet effects were generally more robust in juveniles. The ketogenic diet elevated plasma ketones similarly in both age groups, but caused slowed body growth only in juveniles. These data suggest that applying a ketogenic diet or exploiting cellular mechanisms associated with ketone-based metabolism offers new therapeutic opportunities for controlling pain and peripheral inflammation, and that such a metabolic strategy may offer significant benefits for children and adults.

PMID:

20041135

[PubMed – indexed for MEDLINE]

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