Friday, August 22, 2008

Dr. Larry McCleary - ASDs: Time is of the Essence!

Dr. Larry McCleary - ASDs: Time is of the Essence!

ASDs: Time is of the Essence!
6/30/2008 11:52 PM MST

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Autistic Spectrum Disorders (ASDs) are neurodevelopmental disorders that have much better outcomes the earlier they are diagnosed.and the sooner children are enrolled in appropriate intervention programs. To help disseminate information to more effectively avoid a delayed diagnosis it important to make available some of the earliest signs and symptoms to watch for.

The Child Neurology Service "red flags" screening parameters include the following as absolute indications for immediate evaluation for autism:

1) no babbling or pointing or other gesturing by 12 months of age

2) no single words by 16 months

3) no spontaneous 2-word phrases by 24 months

4) loss of language or social skills at any age

Speech delays usually prompt parents to raise concerns with their child's pediatrician at 16 to 19 months. However, certain social deficits occur earlier and may be more specific but more difficult to recognize. Presenting symptoms can vary widely from one child to the next. Some may be perceived by parents as just "being different" during the first few months of life. Inability to manifest social relatedness by developing connections with others and sharing complementary states is common. These children are content being alone, ignore their parents bids for attention, and seldom make eye contact or bid for other's attention with gestures or vocalizations.

Difficulty with skills such as joint activity is a distinguishing characteristic of very young children with autism. Joint activity refers to the behavior whereby the infant shows enjoyment in sharing an object or an experience with another person by looking back and forth between the two. Early in life it frequently appears as joyous smiling in recognition of a parent's attention or vocalization. At about 8 months of age, an infant starts to follow a parent's gaze and look in the same direction. At 10-12 months children begin to look in the same direction when a parent points at an interesting object. This is usually accompanied by the child looking back at the parent as if to acknowledge a shared appreciation. At 12 to 14 months children typically begin to initiate pointing themselves usually to request a desired object and then to draw the parent's attention to share an interesting object. These pointing episodes are frequently accompanied with a back and forth gaze of the child between the object and the parent in effect to "share" the experience. Orienting to social stimuli such as turning consistently to respond to one's name is an early (8-10 months) trait that is often deficient.

Most children later diagnosed with autism are sent to their doctor for "speech delay." Most parents sense that something is wrong by 18-20 months. Earlier pre-speech deficits often exist and should be looked for. These traits include:

1) lack of appropriate gaze

2) lack of warm, joyful expressions

3) lack of the alternating to-and-fro pattern of vocalizations between infant and parent that usually occurs at approximately 6 months of age (ie, infants with autistic tendencies usually continue vocalizing without regard for the parent's speech)

4) lack of recognition of parent's voice

5) disregard for vocalizations such as calling of the child's name but with preserved awareness of environmental sounds

6) delayed onset of babbling past 9 months

7) decreased use of pre-speech gestures such as waving or pointing

8) lack of expressions such as "oh oh" or "huh"

9) Lack of interest or response of any kind to neutral statements such as "Oh no, it's raining again!"

If you see these changes, please suggest that the child be evaluated as soon as possible because an early, proper diagnosis means starting treatment at a time when the intervention is likely to result in a better outcome for the child.

Killer Carbs - Appetite Control Cells Deteriorate As We Age, Says Study | Scientific Blogging

Killer Carbs - Appetite Control Cells Deteriorate As We Age, Says Study | Scientific Blogging

Killer Carbs - Appetite Control Cells Deteriorate As We Age, Says Study


Dr Zane Andrews, a neuroendocrinologist with Monash University's Department of Physiology, says he has discovered key appetite control cells in the human brain degenerate over time, causing increased hunger and potentially weight-gain as we grow older.

Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars.

"The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more," Dr Andrews said.

Dr Andrews said the attack on appetite suppressing cells creates a cellular imbalance between our need to eat and the message to the brain to stop eating.

"People in the age group of 25 to 50 are most at risk. The neurons that tell people in the crucial age range not to over-eat are being killed-off.

"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMC's kick in.

"However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied," Dr Andrews said.

The free radicals also try to attack the hunger neurons, but these are protected by the uncoupling protein 2 (UCP2).

Dr Andrews said the reduction in the appetite-suppressing cells could be one explanation for the complex condition of adult-onset obesity.

"A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration," Dr Andrews said.

Dr Andrews' next research project will focus on finding if a diet rich in carbohydrates and sugars has other impacts on the brain, such as the increased incidences of neurological conditions like Parkinson's disease.

Quick-burning Carbs May Cause Fatty Liver: Low-glycemic Diet Protected Mice

Quick-burning Carbs May Cause Fatty Liver: Low-glycemic Diet Protected Mice

Quick-burning Carbs May Cause Fatty Liver: Low-glycemic Diet Protected Mice

ScienceDaily (Sep. 27, 2007) — Diets rich in rapidly-digested carbohydrates not only expand waistlines, but may also cause fatty liver, a condition that can lead to liver failure and death, finds a new study in mice.
See also:
Health & Medicine

* Obesity
* Diet and Weight Loss
* Liver Disease

Plants & Animals

* Food
* Mice
* Extreme Survival

Reference

* South Beach diet
* Glycemic index
* Detox diet
* Whole grain

If confirmed in humans, the findings suggest that fatty liver disease -- on the upsurge among Americans as a byproduct of the obesity epidemic -- may be preventable and possibly treatable through dietary changes.

The researchers, led by David Ludwig, MD, PhD, director of the Optimal Weight for Life program at Children's Hospital Boston, fed mice either a high- or a low-glycemic index diet. High-glycemic index foods, including white bread, white rice, most prepared breakfast cereals and concentrated sugar, raise blood sugar quickly. Low-glycemic index foods, like most vegetables, fruits, beans and unprocessed grains, raise blood sugar slowly.

On the high-glycemic index diet, mice ate a type of cornstarch that is digested quickly whereas on the low-glycemic index diet, mice ate a type of cornstarch that is digested slowly. The diets had equal amounts of total calories, fat, protein, and carbohydrate, and the mice were otherwise treated identically.

After six months, the mice weighed the same. However, mice on the low-glycemic index diet were lean, with normal amounts of fat in throughout their bodies. Mice on the high-glycemic index diet had twice the normal amount of fat in their bodies, blood and livers.

When sugar melts out of high-glycemic index food, Ludwig explains, it drives up production of insulin, which tells the body to make and store fat. Nowhere is this message felt more strongly than in the liver, because the pancreas, which makes insulin, dumps the hormone directly into the liver, where concentrations can be many times higher than in the rest of the body. Fat buildup in the liver, or fatty liver, is usually symptomless, but it increases the risk for liver inflammation, which can progress to hepatitis and, in some cases, liver failure.

Fatty liver is becoming more common in Americans, especially in children, says Ludwig. Many cases in adults can be explained by alcoholism, but not the pediatric cases. Where just one case of fatty liver was reported in children in 1980, now between 1 in 4 and 1 in 2 overweight American children are estimated to have the condition. As these millions of children age, some will progress to full-blown liver disease.

"This is a silent but dangerous epidemic," says Ludwig. "Just as type 2 diabetes exploded into our consciousness in the 1990s, so we think fatty liver will in the coming decade."

A previous study found that Italians who ate higher-glycemic index diets had fattier livers, but the study wasn't tightly controlled. The new study makes clear that the type of carbohydrate can cause fatty liver in animals, independent of other elements of diet or lifestyle.

"Our experiment creates a very strong argument that a high-glycemic index diet causes, and a low-glycemic index diet prevents, fatty liver in humans," says Ludwig.

Ludwig and colleagues now hope to confirm this in a just-launched clinical trial -- and to show that a low-glycemic index diet can reverse fatty liver in overweight children. The children, aged 8 to 17, will be randomized to either the low-glycemic diet or a low-fat diet.

Low-fat diets are currently the standard treatment, Ludwig says, but many children with fatty liver don't respond to them. "We think it is a misconception that the fat you're eating goes into the liver," he says.

Ludwig hypothesizes that obesity, sedentary lifestyles and increased consumption of refined carbohydrates are "synergistically" fueling a fatty liver epidemic in children. Ironically, low-fat diets have only made matters worse, replacing fat with sugar or starchy foods that actually increase fat deposition in the body.

"Two low-fat Twinkies, billed as a health food, contain the same amount of sugar as an oral glucose tolerance test -- a test used to determine how much sugar someone can digest," Ludwig says. He notes that the French delicacy pate de fois gras -- the fatty liver of a duck or goose -- is produced by over-feeding the animals with high-glycemic index grains.

Fast-Acting Carbs May Hasten Vision Loss Over Time

Fast-Acting Carbs May Hasten Vision Loss Over Time

Fast-Acting Carbs May Hasten Vision Loss Over Time

ScienceDaily (Dec. 1, 2007) — Consuming higher-than-average amounts of carbohydrates that cause blood sugar levels to spike and fall rapidly could be a risk factor for central vision loss with aging.
See also:
Health & Medicine

* Diet and Weight Loss
* Nutrition
* Healthy Aging

Mind & Brain

* Dieting and Weight Control
* Nutrition Research
* Perception

Reference

* South Beach diet
* Glycemic index
* Whole grain
* Diabetic diet

The study was led by Chung-Jung Chiu with Allen Taylor, both at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) in Boston, Mass. Taylor is director of the Laboratory for Nutrition and Vision Research at the HNRCA.

The researchers analyzed dietary intake and other data from more than 4,000 men and women aged 55 to 80 participating in the Age-Related Eye Disease Study, or AREDS.

Diets high in carbohydrates that are quickly digested and absorbed, resulting in a rapid rise in blood sugar levels, are considered high-glycemic-index diets. Examples of such "fast carb" foods are white bread, rice, potatoes and pasta, and also sugars and corn syrups. Carbohydrates leading to a more gradual rise and fall in blood sugar levels comprise low-glycemic-index diets. Such "slow carb" foods include whole-grain versions of bread, rice and pasta.

Central vision loss is one of the first signs of age-related macular degeneration (AMD), a disease that is one of the leading causes of blindness among the elderly.

Consuming a diet high in fast carbs is also suspected of being involved in the vision loss that sometimes occurs in people with diabetes. The researchers theorize that the type of damage to eye tissue produced by fast carbs could be similar in both AMD and diabetic eye disease.

At this time, there is no effective cure for AMD, so finding modifiable risk factors is important. While it's too soon to recommend dietary slow carbs as a preventive strategy for AMD, replacing fast carbs with whole grains may soon prove to be an early dietary intervention to slow its progression.

Scientists supported by the Agricultural Research Service (ARS) and grants reported the findings this year in the American Journal of Clinical Nutrition.

Killer Carbs: Scientist Finds Key To Overeating As We Age

Killer Carbs: Scientist Finds Key To Overeating As We Age

Killer Carbs: Scientist Finds Key To Overeating As We Age

ScienceDaily (Aug. 22, 2008) — A Monash University scientist has discovered key appetite control cells in the human brain degenerate over time, causing increased hunger and potentially weight-gain as we grow older. The research by Dr Zane Andrews, a neuroendocrinologist with Monash University's Department of Physiology, has been published in Nature.
See also:
Health & Medicine

* Obesity
* Diet and Weight Loss
* Nutrition

Mind & Brain

* Dieting and Weight Control
* Nutrition Research
* Disorders and Syndromes

Reference

* Appetite
* Sensory neuron
* High fructose corn syrup
* Blood sugar

Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars.

"The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more," Dr Andrews said.

Dr Andrews said the attack on appetite suppressing cells creates a cellular imbalance between our need to eat and the message to the brain to stop eating.

"People in the age group of 25 to 50 are most at risk. The neurons that tell people in the crucial age range not to over-eat are being killed-off.

"When the stomach is empty, it triggers the ghrelin hormone that notifies the brain that we are hungry. When we are full, a set of neurons known as POMC's kick in.

"However, free radicals created naturally in the body attack the POMC neurons. This process causes the neurons to degenerate overtime, affecting our judgement as to when our hunger is satisfied," Dr Andrews said.

The free radicals also try to attack the hunger neurons, but these are protected by the uncoupling protein 2 (UCP2).

Dr Andrews said the reduction in the appetite-suppressing cells could be one explanation for the complex condition of adult-onset obesity.

"A diet rich in carbohydrate and sugar that has become more and more prevalent in modern societies over the last 20-30 years has placed so much strain on our bodies that it's leading to premature cell deterioration," Dr Andrews said.

Dr Andrews' next research project will focus on finding if a diet rich in carbohydrates and sugars has other impacts on the brain, such as the increased incidences of neurological conditions like Parkinson's disease.

Wednesday, August 20, 2008

Carbohydrate restriction, prostate cancer growth, ...[Prostate. 2008] - PubMed Result

Carbohydrate restriction, prostate cancer growth, ...[Prostate. 2008] - PubMed Result

Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis.
Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB.

Department of Surgery, Durham VA Medical Center, Durham, North Carolina 27710, USA. steve.freedland@duke.edu

BACKGROUND: Recent evidence suggests carbohydrate intake may influence prostate cancer biology. We tested whether a no-carbohydrate ketogenic diet (NCKD) would delay prostate cancer growth relative to Western and low-fat diets in a xenograft model. METHODS: Seventy-five male SCID mice were fed a NCKD (84% fat-0% carbohydrate-16% protein kcal), low-fat (12% fat-72% carbohydrate-16% protein kcal), or Western diet (40% fat-44% carbohydrate-16% protein kcal). Low-fat mice were fed ad libitum and the other arms fed via a modified-paired feeding protocol. After 24 days, all mice were injected with LAPC-4 cells and sacrificed when tumors approached 1,000 mm(3). RESULTS: Despite consuming equal calories, NCKD-fed mice lost weight (up to 15% body weight) relative to low-fat and Western diet-fed mice and required additional kcal to equalize body weight. Fifty-one days after injection, NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice. Serum IGFBP-3 was highest and IGF-1:IGFBP-3 ratio was lowest among NCKD mice while serum insulin and IGF-1 levels were highest in Western mice. NCKD mice had significantly decreased hepatic fatty infiltration relative to the other arms. CONCLUSIONS: In this xenograft model, despite consuming more calories, NCKD-fed mice had significantly reduced tumor growth and prolonged survival relative to Western mice and was associated with favorable changes in serum insulin and IGF axis hormones relative to low-fat or Western diet. (c) 2007 Wiley-Liss, Inc.

Tuesday, August 19, 2008

A causal role for uric acid in fructose-induced metabolic syndrome -- Nakagawa et al. 290 (3): F625 -- AJP - Renal Physiology

A causal role for uric acid in fructose-induced metabolic syndrome -- Nakagawa et al. 290 (3): F625 -- AJP - Renal Physiology

A causal role for uric acid in fructose-induced metabolic syndrome
Takahiko Nakagawa,1 Hanbo Hu,1 Sergey Zharikov,1 Katherine R. Tuttle,2 Robert A. Short,2,3 Olena Glushakova,1 Xiaosen Ouyang,1 Daniel I. Feig,4 Edward R. Block,1 Jaime Herrera-Acosta,5,{dagger} Jawaharlal M. Patel,1 and Richard J. Johnson1

1Division of Nephrology, Hypertension, and Transplantation, University of Florida, Gainesville, Florida; 2Department of Research, The Heart Institute of Spokane, and 3Biostatistics, Washington State University, Spokane, Washington; 4Division of Nephrology-Medicine, Baylor College of Medicine, Houston, Texas; and 5Departamento de Nefrologia, Instituto Nacional de Cardiologia Ignacio Chavez, Tlalpan, Mexico

Submitted 6 April 2005 ; accepted in final form 26 September 2005

The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.

Dr. Doom - Profile - Nouriel Roubini - Predicting Crisis in the United States Economy - NYTimes.com

Dr. Doom - Profile - Nouriel Roubini - Predicting Crisis in the United States Economy - NYTimes.com

LINK to profile of Roubini in NY Times



The Decline of the American Empire

Nouriel Roubini | Aug 13, 2008

Recent economic, financial and geopolitical events suggest that the decline of the American Empire has started. After the collapse of the Soviet Union there was a brief period where the world switched from a bipolar balance of two superpowers to a unipolar world with one economic, financial, geostrategic superpower, or better, hyperpower, i.e the United States. But by now three factors suggest that the US has squandered its unipolar moment and that the decline of the American Empire – as the US was in effect a global empire – has started.

Let us explain how and why...

First, the US squandered its power by relying excessively on its hard military power in the wars of Iraq and Afghanistan and in its unilateralist foreign policy – including economic issues such as global warming - rather than relying more on its soft power of diplomacy and multilateralist approaches to global policy issues.

Second, regardless of mistaken US policies the rise of other economic and financial powers – the rise of China, the recent resurgence of Russia, the process of economic and political integration in the European Union, the emergence of India, and the rise of other regional powers such as Brazil, South Africa and Iran – implies that the relative economic, financial and geopolitical power of the US will be reduced over time. We are indeed slowly moving towards a multipolar world where there will be a balance of Great Powers rather than the hegemony of a single hyperpower. While on military terms the US is still the only superpower even its military power is now restricted by imperial overstretch and its armed forces being bogged down in Iraq and Afghanistan; thus, Russia has now been able to flex its muscle in its Central Asian backyard and humiliated the US – not just Georgia – in the latest conflict on South Ossetia. For the Bush administration having supported Georgia by words only and show its impotence – or unwillingness - to support an ally in spite of the administration push to have Georgia join NATO shows the limits of the American power. The US is at fault for effectively letting Georgia start a reckless attack on South Ossetia. Russia has scary and dangerous neo-imperial goals but deeply flawed US foreign policy of encircling a paranoid Russia allowed the worst nationalist tendencies of the Russian bear to reemerge.

Third, and more important, the US squandered its economic and financial power by running reckless economic policies, especially its twin fiscal and current account deficits. The last time around the current account started to go into negative territory in 1991 after a brief surplus during the 1990-91 recession. In the 1990s the growing US current account deficit was driven by a private investment boom – the internet technological revolution – and thus the accumulation of foreign liabilities of the US was driven by FDI and M&A activity, i.e the US accumulated foreign liabilities in the form of equity rather than debt. But since 2001 the further worsening of the US current account deficit was driven instead by growing fiscal deficits - especially in the 2001-2004 period – caused by unsustainable tax cuts and by the buildup of spending on foreign wars and on domestic security and since 2002 by the collapse of household savings and boom in investment in unproductive stock of housing capital that the housing bubble induced. And while the weak dollar is now inducing a modest improvement of the external deficit the looming sharp increase in fiscal deficits - that the current recession and financial crisis is inducing - will cause a return of twin deficits in the coming years. By now the US is the biggest net borrower in the world – running current account deficits still in the 700 billion dollars range – and the biggest net debtor in the world with its foreign liabilities now over 2.5 trillion dollars.

The trouble with these twin deficits is multi-fold.

First, superpowers and empires - like the British Empire at its peak - tend to be net lenders – i.e run current account surpluses – and be net creditors, not net debtors; The decline of the British Empire started in World War II when the British fiscal deficits in the war and the current account deficits turned that empire into a net borrower and a net debtor both in its public debt and external debt. That financial switch into an external debtor and borrower position was also the reason for the decline of the British pound as the leading reserve currency. And the British twin deficits were being financed by a rising economic and financial power that was a net lender and a net creditor, the US.

Second, the last time the US was running large twin deficits in the 1980s the main financers of these deficits were the friends and allies of the US, i.e Japan, Germany and Europe as the US external deficit was against these economies. Today instead the economic powers financing the US twin deficits are the strategic rivals of the US – China and Russia – and unstable petro-states, i.e Saudi Arabia, the Gulf States and other shaky petro-states. This system of vendor financing – with these US creditors providing both the goods being imported and the financing of such deficits – has led to a balance of financial terror: if these creditors were to pull the plug on the financing of the US twin deficits the dollar would collapse and US interest rates would go through the roof.

Third, while it is unlikely that China, Russia and other powers would suddenly pull the rug from under the US feet – as such action would lead to a sharp appreciation of their currency and negatively affect their export led growth model – relying excessively on the kindness of strangers – especially that of your strategic rivals – is extremely risky. Since almost 100 percent of all US fiscal deficits since 2001 have been financed by non-residents – as US residents net holdings of US Treasuries have been flat since 2001 - by now the total stock of US Treasuries held by non-residents is getting close to 60 percent. And the foreign financing of the US current account deficits has also become more risky: less FDI and equity, more debt, more short term debt, more debt held by official political actors – central banks and sovereign wealth funds – , less debt held by foreign private investors, and more debt held by politicals rivals rather than allies of the US. This change makes the US vulnerable to such rivals using the financial terror weapon – dumping US assets and or reduicing their financing of the US twin deficits – in situations of geostrategic tension.

Suppose Russia flexes further its muscle in its backyard – under the pretense of defending abused Russian minorities in Ukraine, the Baltics and other former Soviet Union or Iron Curtain countries. Then Russia could use its financial power – the ability to dump hundreds of billions of dollar assets – to exert both financial and military influence. So could China over time if trouble in Taiwan or other disputed Asian territories become big geopolitical issues. Russia and China are already winning the new war for the control of commodities and ressources through their investments in Africa and Latin America - in the case of China – and its domestic and foreign control of energy and pipelines in Central Asia in the case of Russia. China and Russia are indeed winning the new Scramble for Resources.

Fourth, the foreign creditors of the US are getting tired of financing the US in the form of low-yielding US Treasuries. Thus the switch of such reserve holdings to SWFs that are planning to make large equity investments possibly with actual control of corporate firms and financial institutions that are desperate for capital to recapitalize themselves. But this desire of our creditors to get equity investments – the gems of the US corporate world - rather than low yield debt instruments is hitting the political backlash of financial protectionism as the UNOCAL- CNOOC, the Dubai Ports cases and the likely protectionist reform of the CIFIUS process of approving FDI in the US suggest. But a country that needs to borrow from abroad 700 to 800 billion dollar a year to finance its external deficit cannot afford to be too choosy on the ways – equity rather than debt – that its lenders and creditors want to finance those deficits. The first rule of good manners if you are a guest is that you don't spit on the plate from which your host is feeding you. But in its creeping financial protectionism the US thinks it can dictate to other countries the form and the terms of the financing of its twin deficits. This attitude will not be allowed by such creditors to last much longer.

The ensuing decline of the US dollar as the main reserve currency will take time and will not occur overnight; but it is inexorable given the relative fall in US economic, financial and geopolitical power. Already Russia is flexing its muscle and pushing for an international role of the ruble; the euro is rising as a major reserve currency; central banks and SWFs will slowly but surely start to diversify away from dollar assets especially as the Bretton Woods 2 regime starts to unravel; and even the RMB may become the dominant currency in Asia in the next decade as capital controls are slowly removed in China. It will take little time – if the secular decline of the value of the dollar continues – for oil and other commodities to be priced in currencies other than the dollar or in a basket of currencies.
All these changes in the economic, financial, reserve currency and geopolitical role and relative power of the US will not occur overnight. But the trend is clear. The rise of the BRICs and other emerging market economies; the continuation of the process of economic and political integration in Europe; the US policy mistakes in economic, financial and foreign policies will steadily erode the power of the American Empire. This process will not be sudden and will take a couple of decades. But the trend is clear: the brief period of unipolar power of the American hyperpower is now over and a new age of balance of great powers is starting in the world. Also, the rise of non governmental actors – multinational corporations, NGOs, terrorist groups, non-nation state powers, failed and unstable states, non-traditional global players – will radically change the traditional balance of power as the power of nation states will shrink relative to that of other global players.
Whether the decline of an hegemonic power providing global public goods – security, free trade, freer mobility of capital and people, inducements to free markets and democracy, better environment, peace – will lead to a more stable world with many powers multilaterally cooperating on these global economic, financial and geopolitical issues; or whether the absence of such stable hegemonic power will lead to a more unstable world characterized by conflicts – economic, political and even military – among traditional nation states, great powers and non-traditional actors is an open and difficult issue. But it is certain that the decline of the American Empire has started.

Monday, August 18, 2008

‘Sugar Fix’ Author Blames Fructose Alone For Obesity, But Taubes Counters

‘Sugar Fix’ Author Blames Fructose Alone For Obesity, But Taubes Counters

‘Sugar Fix’ Author Blames Fructose Alone For Obesity, But Taubes Counters
Jimmy Moore
August 7, 2008

The following is a reprint from the blog "Livin' La Vida Low-Carb":


Is it really just fructose that’s making us fat and unhealthy?

In an effort to keep things understandable by the average person visiting my blog, I like to keep things as simple as they can possibly be. You and I both know not everything is so black and white, but the trick is to get people at least thinking about a subject and hopefully digging deeper on their own to learn even more about it. That’s the essence of learning–get armed with a little truth and then investigate it further and further until comprehension takes place.

One such simplistic subject you often see me blog about is sugar. Yes, there’s that sweet-tasting white stuff known as sucrose, or table sugar, that millions of Americans put in their food and drinks each day without any regard for what it is doing to their bodies. An equally if not MORE harmful sugar is the evil high-fructose corn syrup that is showing up in about 90 percent of packaged foods these days. Food manufacturers made the switch from sucrose to fructose in the 1970s and our weight and health has suffered ever since.

That’s why I think it is awesome to see books coming out from major publishers blowing the horn on the harmful impact that sugar, both in the form of sucrose and fructose, is having on us. One such book that looked to be promising was the April 2008 release from Rodale called The Sugar Fix: The High-Fructose Fallout That Is Making You Fat and Sick by Dr. Richard Johnson. On face value, it sounds like a good book for people who are livin’ la vida low-carb to read. We pretty much all agree fructose is bad news and should be avoided.

Questions linger about what role sucrose and even sugar that is produced by starchy carbohydrates play in obesity and disease. Dr. Johnson apparently does not address this in his book and that had one of my readers very concerned. Although I have not yet read this book (but would like to!), this very concerned reader says now he’s confused.

After he read Gary Taubes’ masterpiece Good Calories Bad Calories where insulin was identified as the source of obesity and disease, not just fructose, he’s left scratching his head about what the truth is. In his e-mail to me, the reader asked if I would forward on his questions to Taubes for a response. Below you will see both the reader’s original e-mail to me and Gary Taubes’ reply:

Hey Jimmy, I know you must get a million emails a day, but here’s one more! I just finished reading a new book called The Sugar Fix.

And now I’m REALLY confused. I thought it would be a low-carb message, but it ended up being a low-FRUCTOSE message with the “calorie is a calorie” theory underpinning it. The author Richard Johnson, who is a medical researcher and a kidney transplant doctor (so he should know his stuff), claims that it is only the fructose in our diets that makes us fat and sick.

Following his logic, because sucrose is half fructose and high-fructose corn syrup (HFCS) contains a lot of fructose, all we need to do to be healthy and lose weight is cut out the fructose in our diets. Practically, of course, this means cutting out all drinks sweetened with sugar and HFCS, and cutting down on table sugar, honey, sweet desserts, etc. What really confuses me is that he claims that starch is not a problem.

He says in this book that insulin resistance is caused by FRUCTOSE, not glucose, and that glucose alone causes insulin to spike, but in the absence of fructose, it will not influence insulin resistance in the slightest. So according to this book, if you have your fructose under control (including fruit only in moderation), then you can still enjoy potatoes, pasta and breads because glucose from starch is not a problem.

Now, I’m going through Good Calories Bad Calories for a third time and Gary Taubes argues convincingly that INSULIN is the problem and leads to weight gain and sickness. You see why I’m confused? The author of The Sugar Fix quotes all the studies, is a researcher himself, and now I don’t know WHAT to think.

I thought you would find this interesting, but the real reason I’m telling you all this is that I’m hoping you might pass this note on to Gary Taubes. I would LOVE to hear from him on this, and I know you are in contact with him. His book has been extremely influential in my life, but now I’m having some doubts. THANKS!

And now here is what Gary Taubes had to say in response:

I interviewed Richard Johnson, the author of The Sugar Fix, for my book and have spoken to him a lot since his book came out. He is now trying to get a paper published arguing that fructose and thus sugar and HFCS are the environmental causes of diabetes and metabolic syndrome.

He only read my book after The Sugar Fix was published, so the argument that obesity is not caused by excess calories never made it into his book. That said, it still isn’t in his paper either, so he either doesn’t understand it fully or doesn’t buy it, which is fair enough. Although Dr. Johnson gives my book a very complimentary acknowledgment in the paper he’s trying to get published, I still think he labors under one of the problems I suggest is endemic in the medical research community: that he focuses too tightly on the subject of his own research and doesn’t look far enough outside of it to see what other factors might be involved.

Dr. Johnson does talk about the ability of fructose to stimulate fat synthesis in the liver and, at least indirectly, on its ability in the long term to cause insulin resistance, which, if I’m right, would still be the fundamental cause of weight gain. He’s primarily interested in the ability of fructose to elevate uric acid levels, which could be a causal agent, as well, in causing metabolic disorders in heart disease, obesity and diabetes.

I didn’t get into this in the book because the literature is very sparse and the book was already too long and technical. The fundamental problem here is differentiating between the effect of excess calories and the effect of the nutrient itself on fat deposition, thus allowing for the consumption of excess calories. Dr. Johnson argues that its not possible to induce insulin resistance in animal models by feeding them glucose alone–starches–and can only be done by giving them fructose. Or that it happens far more quickly with fructose than glucose alone. That may be true.

As I say in Good Calories Bad Calories, there is reasonable evidence that sugar is the fundamental problem. But that hypothesis has to be rigorously tested. It’s virtually impossible to find populations that consume refined carbs but not sugars. And, indeed, most populations that are used as counter examples to the carb-insulin hypothesis are those that consumed virtually no sugar–the Japanese, Koreans, etc.

The counter-argument is the one that Peter Cleave made in the 1960s, which is where you can find a lot of extremely fat people who eat no sugar at all but drink a lot of beer, which is another kind of refined carb/sugar–in this case, maltose.

There are four questions here that are key, and I don’t think any can be answered definitively: 1) is fructose alone the problem? 2). Is it worse or particularly noxious, as I suggest in the book, when it’s packaged with glucose, as it is in sugar and HFCS? 3) Does this mean high-glycemic index carbohydrates–white flour and white rice, for instance–are relatively harmless if fructose and so sugar and HFCS is not in the diet? And once sugar and HFCS have caused, say, obesity, metabolic syndrome and diabetes, can you cure the problem only by removing the fructose, but not the glucose?

One possibility, for instance, is that fructose and glucose are needed to create chronically elevated insulin levels and so cause weight gain, metabolic syndrome, etc., but that once the process is initiated all easily digestible carbohydrates keep it going or make it worse. What’s needed is a research community that takes all these hypotheses seriously and then sets out to find out the answers.

One other point to keep in mind is that there are diets out there that limit fructose dramatically–the DASH diet, for instance, that’s now being pushed to treat hypertension. It’s got virtually no sugar in it, but is still relatively high-carb. It does reduce blood pressure, which would be expected. There’s no reason to believe, though, that it drops weight as dramatically as the Atkins diet can, and Atkins restricts all carbs.

So I think Dr. Johnson’s hypothesis is very interesting and potentially very valuable, if it further directs attention to the potential dangers of sugar and HFCS, but I also think it’s too narrow and misses the effect of other carbohydrates, which also elevate insulin levels. I hope all this helps.

What do you think about all of this? As Taubes states in his response, these are the kinds of questions that the research community should be all over taking a serious look at for the sake of finding the answers for people like my reader who are confused. Unfortunately, most people just look at sugar as sugar regardless of its form and consume it liberally without any regard for what they are doing to themselves. They’re freaked out by eating fat, but sugar has to be okay because it tastes so good.

When did our world turn upside down? I look forward to your comments!

Sunday, August 17, 2008

Suspect in U.S. obesity epidemic - Op-Ed - Kentucky.com

Suspect in U.S. obesity epidemic - Op-Ed - Kentucky.com

Suspect in U.S. obesity epidemic
Shirley Caudill
Contributing columnist

More than 33 percent of adults in the United States are overweight or obese.

The incidence of obesity in children and adults has doubled in the last 10 years, but parents are at a loss as to the cause of this problem in their children.

New research has found evidence that soft drinks sweetened with high-fructose corn syrup may contribute to the development of diabetes and obesity, especially in children.

Scientists found that drinks with corn syrup have high levels of reactive compounds that have been shown to have the potential to trigger cell and tissue damage that could cause the disease, which is at epidemic levels. The findings were reported at the 234th national meeting of the American Chemical Society last August.

According to Meira Field of the U.S Department of Agriculture, most processed foods contain corn syrup. The sweetener is found in many foods and beverages, from soda, baked goods and condiments to so-called health foods. It has become manufacturers' sweetener of choice because it is cheaper, sweeter and more easily blended than granulated white sugar.

The food industry disputes the findings, but some researchers suggest that high fructose sweeteners increase the risk of obesity and diabetes. In a current study, a scientist conducted chemical tests on 11 different soft drinks containing high-fructose corn syrup, and he found ”astonishingly high“ levels of reactive carbonyls in those drinks.

Such high levels of these highly reactive compounds associated with ”unbound“ fructose and glucose molecules are believed to cause tissue damage, said Chi-Tang Ho, a professor of food science at Rutger's University.

Saturday, August 16, 2008

Vaporizing.Info - Medical Uses of Cannabis

Vaporizing.Info - Medical Uses of Cannabis

Diabetes: Insulin is excreted from the beta islet cells of the pancreas. Insulin, a natural body chemical, floods the body after a sugar-rich meal and causes various cell types to dramatically increase their uptake of glucose, a common sugar. The effect of insulin is to reduce the levels of glucose in the bloodstream. Diabetes can result from the body's inability to produce sufficient quantities of insulin or from an inability to respond properly to the insulin that is produced. In either case, many of the clinical effects of diabetes stem from the deleterious effects of high blood sugar.

There is some anecdotal evidence that Cannabis lowers blood sugar. AIDS and cancer patients, among other Cannabis users, often report an increase in appetite after consuming Cannabis, and a few reports indicate that smoking Cannabis can lower blood sugar in diabetics.

A study (Tracy Blevins phd) was undertaken to determine whether this effect can be detected using an easily available over the counter blood glucose testing kit.

A morbidly obese man had a non-healing wound on his lower leg and was experiencing confusion and sleepiness after large meals. He suspected diabetes as the culprit, and, since smoking a large Cannabis cigarette after large meals seemed to alleviate some of his symptoms, his blood sugar was tested before, immediately after and multiple times during the hour following a large meal rich in protein, fats and both complex and simple carbohydrates.

The results were dramatic and raised some interesting research questions. Before and immediately after the meal, the patient's blood sugar was in the normal range, but within a few minutes increased by 80 mg/dl and remained at this high level for almost an hour. Then he smoked a 1 gram Cannabis cigarette, and his blood sugar levels fell by 40 points almost instantly. This represents a full 50% of the abnormal increase in blood sugar.

The drop of blood which was taken at the exact moment when he was self reporting a ‘high' were the lowest in blood sugar, a good indication that the blood sugar lowering was caused by the ingestion of Cannabis. Curiously, after a few minutes, his blood sugar started to increase again. It might be that smoking Cannabis helped to reduce his blood sugar, but only transiently. Would a longer acting cannabinoid suppress blood sugar levels more efficiently?

Further studies are necessary to confirm this effect and to determine the parameters of the effect: the amount of Cannabis needed, the time course of the effect, and also whether different types of Cannabis show more or less blood sugar lowering. Also, in another non-diabetic patient, blood sugar was decreased by 11%, pointing to the possibility that Cannabis can lower blood sugar in a non-disease state. Could it be that we have finally discovered the biological mechanism of “the munchies”?

Thursday, August 14, 2008

Alcoholism may be controlled with nutrient therapy | Better Nutrition (1989-90) | Find Articles at BNET

Alcoholism may be controlled with nutrient therapy | Better Nutrition (1989-90) | Find Articles at BNET

Research into the genetics of alcoholism has taken off the last 15 years and has produced a great body of information blaming the disease on everything from tainted genes to permissive parents. Yet the consistent rate of failure in treating alcoholics has motivated some health experts to look at nutritional approaches. Some researchers suggest that alcoholism may, in some cases, actually result from hypoglycemia and nutritional deficiencies. For years, physicians believed that hypoglycemia resulted when alcohol was consumed in preference to food. However, according to Carl Pfeiffer, M.D., Ph.D., author of Mental and Elemental Nutrients, evidence suggests that many nutritional disorders, hypoglycemia in particular, actually precede alcoholism.

An experiment performed on rats confirmed this view. One group of rats was fed a refined carbohydrate diet known to cause hypoglycemia. Another group was fed unrefined carbohydrates and supplemental vitamins. A third was given a high-protein, unrefined-carbohydrate diet, typically used to treat hypoglycemia. Each group was given two drinking sources: water and alcohol. The group fed refined carbohydrates slowly began to prefer the alcohol until they eventually shunned water almost completely. The low-protein group drank a little alcohol, while the third group avoided the alcohol altogether.

According to Dr. Ross Trattler, a naturopath and osteopathic physician, although the original causes of drinking may be social, a dependence on alcohol is the start of a vicious cycle. "He or she drinks to relieve standard hypoglycemic symptoms of depression, tension, irritability, tiredness, inability to think and so on. The alcohol gives a blood sugar boost which acts as positive reinforcement, along with a reversal of the unpleasant hypoglycemic sensations."

Tuesday, August 12, 2008

Alcohol Vulnerability Linked To Action Of Insulin

Alcohol Vulnerability Linked To Action Of Insulin"This finding opens promising new avenues for the treatment of alcoholism," said Ulrike Heberlein, PhD, UCSF professor of anatomy and senior author on the paper. "Insulin is already known to act in the nervous system to regulate food intake, so it makes sense that it would influence the response to other substances the body senses as rewards, such as alcohol or drugs of abuse."

Insulin functions in the brains of animals from worms to mammals, and the pathway by which it influences behavior has been conserved throughout millions of years of evolution, Heberlein said, and research has recently revealed that insulin reduces the presence of the molecule that transports dopamine in the brain.

"In animals and humans, dopamine in the brain affects the response to both food and drugs. We are starting to see that in addition to its importance in sugar metabolism, insulin regulates release of neurotransmitters and may be crucial in determining the response to addictive drugs."

Monday, August 04, 2008

My Way News - Martian soil may contain detrimental substance

My Way News - Martian soil may contain detrimental substance

NASA's Phoenix spacecraft has detected the presence of a chemically reactive salt in the Martian soil, a finding that if confirmed could make it less friendly to potential life than once believed.

Scientists previously reported that the soil near Mars' north pole was similar to backyard gardens on Earth where plants such as asparagus, green beans and turnips could grow. But preliminary results from a second lab test found perchlorate, a highly oxidizing salt, that would create a harsh environment.

The first test "suggested Earth-like soil. Further analysis has revealed un-Earthlike aspects of the soil chemistry," chief scientist Peter Smith of the University of Arizona in Tucson said in a statement Monday.

On Earth, perchlorate is a natural and manmade contaminant sometimes found in soil and groundwater. It is the main ingredient in solid rocket fuel and can be found in fireworks, pyrotechnics and other explosives.

It's unclear how perchlorate forms on Mars or how much there is of it. NASA is investigating whether the substance could have gotten there by contamination before launch. Phoenix used another fuel, hydrazine, to power its thrusters and land on the red planet on May 25.

[...]

Scientists want to confirm their results because another Phoenix instrument that bakes and sniffs soil samples found no evidence of perchlorate during a run on Sunday.

Brown University geologist John Mustard, who has no role in the mission, said judgment about the soil's potential to support life should be reserved until all the data are in.

But at first glance, "it is a reactive compound. It's not usually considered an ingredient for life," Mustard said.

Saturday, August 02, 2008

Stand Up For Your Health -- Physiologists And Microbiologists Find Link Between Sitting And Poor Health

Stand Up For Your Health -- Physiologists And Microbiologists Find Link Between Sitting And Poor Health

Physiologists analyzing obesity, heart disease, and diabetes found that the act of sitting shuts down the circulation of a fat-absorbing enzyme called lipase. They found that standing up engages muscles and promotes the distribution of lipase, which prompts the body to process fat and cholesterol, independent of the amount of time spent exercising. They also found that standing up uses blood glucose and may discourage the development of diabetes.

You're probably sitting down right now. Well, by the time you're done reading this, you may see sitting in a whole new way!

"Chair time is an insidious hazard because people haven't been told it's a hazard," Marc Hamilton, Ph.D., a professor of biomedical sciences at the University of Missouri in Columbia, told Ivanhoe.

That's right -- the time you sit in your chair could be keeping your body's fat burning in park! More than 47 million adults in the United States have metabolic syndrome, which causes obesity, diabetes and heart disease. Biomedical researchers from the say the reason so many of us have the condition is because we sit too much!

"The existing data, by numerous studies, are starting to show that the rates of heart disease and diabetes and obesity are doubled or sometimes even tripled in people who sit a lot," Dr. Hamilton explains. One reason, he says, is an enzyme called lipase. When it's on, fat is absorbed into the muscles, but when we sit down, lipase virtually shuts off.