Daily Mail, 30 Apr 2008. Page 3

Pill that lets you eat what you like without piling on weight

By Fiona MacRae Science Reporter

IT is every dieter’s dream – a pill that allows you to lose weight safely without actually going on a diet.

But such fat-fighting drugs are already the stuff of reality, according to researchers.

They say tablets widely used to lower blood pressure could help melt away unwanted pounds as well.

Experiments suggest that ACE inhibitor pills can speed up the metabolism, allowing excess weight to be lost quickly.

The findings could lead to the pills, taken by millions to combat hypertension, being repackaged as fat-burners.

Ultimately, they, or similar drugs, could allow the overweight to shed flab without even setting foot in a gym. With up to a quarter of Britons thought to be trying to lose weight and obesity rates the highest in Europe, such a pill would have mass appeal.

Australian researchers made the breakthrough in experiments on mice genetically altered to lack an enzyme found in fat cells.

Those lacking this angiotension converting enzyme, as it is known, weighed 20 per cent less than other mice and had up to 60 per cent less body fat.

The GM mice were no more active than the other creatures and ate just as much food but their metabolism was faster.

They also processed sugar more quickly, suggesting they were at lower risk of diabetes, says a report in the journal Proceedings of the National Academy of Sciences.

The finding raises the possibility that drugs that block the enzyme, such as blood pressure-lowering ACE inhibitors, could be used to help humans lose weight.

Warning that more work needs to be done before the prescription only pills are used to fight fat, researcher Dr Michael Matthias said: ‘The drugs are out there because they are used for hypertension.

‘So we know their safety and their tolerability. What we don’t know is whether or not they will work in humans.’

The researcher, from Melbourne University, told BBC Radio 4’s Today programme: ‘I don’t think this will replace the need for careful control of diet and encouraging more exercise.

‘If people look at increasing their food intake then all that will do is cancel out the beneficial effects of increasing metabolic rate.’

Dr Ian Campbell, medical director of the British charity Weight Concern, said: ‘All the evidence we have is that nothing works better than a healthy diet and increased physical activity, with or without weight loss drugs.’

F.Macrae@DailyMail.co.uk

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Daily Mail
30 Apr 2008

Daily Mail, 29 Apr 2008. Page 44

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Can fasting YourSelf help combat cancer?

Edit [bold] of original article by Medical Correspondent @ The Daily Mail, UK ...


FASTING the body of food for a couple of days could help in the fight against cancer, according to new research.

Scientists have discovered that a 48-hour fast seems to protect the body’s healthy cells against the toxic effects of chemotherapy drugs.

The breakthrough could provide a solution to a problem that has confounded cancer experts for years — how to target chemotherapy so it destroys cancer cells but leaves healthy ones intact.

It seems depriving healthy cells of the food they need for fuel sends them into a kind of survival mode, where they become highly resistant to stress or damage.

Experts describe this behaviour as similar to animals waiting out winter food shortages by hibernating.

But cancer cells do not react in the same way. Instead, they carry on growing and remain just as susceptible to the effects of chemotherapy as they do when the body has a full supply of food.

The result could be that doctors can cure more cancers by using higher doses of chemotherapy drugs to CANCER shrink or destroy tumours.

CANCER affects one in three people in the UK at some point in their lives. Many end up needing a course of chemotherapy to try to control the spread of the disease.

Treatment may involve drugs which block the effects of certain hormones or affect the immune system, but the main group of drugs that are used are called cytotoxics, which mean they poison cells to stop them reproducing.

There are more than 100 different cytotoxic drugs in use for cancer, but none is capable of telling the difference between normal and cancer cells.

Although healthy cells usually recover from the toxic effects of the drugs, they need some time to recuperate.

This means treatment is often given in short bursts, with several weeks’ break in between to allow normal cells cells a chance to recover. But many patients still end up suffering unpleasant side-effects such as hair loss, nausea and extreme tiredness.

If doctors could find a way of protecting healthy cells, they could give patients shorter but more intense bouts of treatment, with fewer adverse effects.

For more than 50 years, there has been evidence that fasting — or limiting calorie intake — can slow the ageing process by switching on some kind of internal protection mechanism in the body.

There is even a Calorie Restriction Society, a U.S.based organisation whose members deliberately limit food intake in an attempt to live longer.

The latest findings, published in the Proceedings of the National Academy of Sciences, suggest that depriving the body of calories in this way could also transform cancer care.

For the study, mice with cancer were fasted for two days before being given a high dose of chemotherapy. Tumour cells were destroyed by the drugs, but the healthy cells survived the treatment intact.

In a separate group of mice that ate 'normally', the treatment killed more than half of them and caused severe weight and energy loss in the survivors.

Laboratory tests suggested fasting had a similarly beneficial effect on human cells. But UK cancer experts have warned patients not to fast themselves until there is more evidence that it works and is safe.

Cancer Research UK science information officer Henry Scowcroft said: ‘This is an interesting result based on solid science and may open up new avenues to improve cancer treatment.

‘But it doesn’t really fit with what we know about chemotherapy, which is that if you are healthy, well-fed and you get enough nutrients you tend to cope with it better.

‘Until these findings are confirmed in human trials, we strongly advise people undergoing cancer treatment to eat a healthy, balanced diet.’

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Daily Mail
29 Apr 2008

Diabetes Cure For Schizophrenia is better than inefficient snacking OR nerve insulinic & glucagonic fitness is better still ...HOW ?

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Med Hypotheses. 2005;65(6):1076-81. Epub 2005 Aug 25.

Links

Impaired neuronal glucose uptake in pathogenesis of schizophrenia - can GLUT 1 and GLUT 3 deficits explain imaging, post-mortem and pharmacological findings?

Emma McDermott, Leeds University, United Kingdom.

Prasanna de Silva, Tees and North East Yorkshire NHS Trust, The Anchorage, 11 Byland Road, Whitby YO21 1JH, United Kingdom

Helen.Clarke@tney.northy.nhs.uk

The largely empirical dopamine theory has limited value in clarifying the pathogenesis of schizophrenia, due to its inability to explain consistent imaging findings, such as cortical grey matter loss, reduced frontal and thalamic activity, and, reduced D1 receptor load.

Furthermore, the most effective drug for treating positive and negative symptoms - clozapine - has minimal dopaminergic activity whilst olanzapine often has substantial HYPERglycemia activity. An alternative HYPO-thesis, therefore, is proposed ... centring on presumed deficits in membrane bound glucose transporter proteins GLUT 1 and GLUT 3, either in absolute numbers or functional capacity.

In situations of high demand, intracellular HYPOglycemia in neurones and astrocytes will produce acute symptoms of misperceptions, misinterpretations, anxiety and irritability - the usual features of prodromal and first onset schizophrenia.

Furthermore, reduced glucose uptake will disrupt production of glutamate--functionally similar to the schizophrenia-like syndrome produced by PCP, a glutamate antagonist.

In the longer term, reduced neuronal growth and poor synaptic contacts will produce chronic cognitive difficulties and perpetuate acute symptoms. A backlog effect due to reduced brain uptake of glucose would produce systemic HYPERglycemia observed in drug naive subjects.

Rat studies have shown that clozapine and similar compounds block GLUT proteins in the brain and peripherally, more so than selective dopamine blockers. By blocking GLUT proteins, clozapine would break malfunctioning circuits, resulting in the disappearance of cognitive and perceptual symptoms.

Unfortunately, these drugs would also raise systemic glucose levels, increasing the risk of diabetes, as observed in longer term studies of clozapine in particular.

This HYPO-thesis summarizes potentially useful research strategies, including studying the genotype of GLUT proteins with respect to schizophrenia phenotypes, activation studies involving fMRI using deoxyglucose as a substrate, and investigating clinical features of Schizophrenic Patients prior to and following treatment for co-existing diabetes.

http://www.ncbi.nlm.nih.gov/pubmed/16125330

Person Emma McDermott

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Daily Mail, 28 Apr 2008. Page 9

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Chocolate study that may not gladden women’s hearts

Edit [bold] of original article by Jenny Hope Medical Correspondent @ The Daily Mail, UK ...

... AS ANY woman could tell you, chocolate can help heal a broken heart. But now scientists have decided to prove it.

They are embarking on a year-long study to test chocolate’s ability to stave off heart disease.

Researchers are seeking volunteers to participate, who must be women who have gone through the menopause, with type 2 diabetes and be taking cholesterol-lowering statin drugs – and need to have a sweet tooth.

The study involves eating a specially-formulated bar containing dark chocolate and SOy every day for a year.

The team at the University of East Anglia [aka UEA] will test the theory that regularly eating dark chocolate and SOy cuts women’s risk of heart problems. Both substances, which contain compounds called flavonoids, are already known to have some heart benefits.

As part of the study, participants will have their risk of heart disease tested five times during the year. Professor Aedin Cassidy, the lead researcher and professor of diet and health at UEA, said: ‘Despite postmenopausal women being at a similar risk to men for developing cardiovascular disease, to date they are under-represented in clinical trials.

‘We hope to show that adding flavonoids to their diets will provide additional protection from heart disease and give women the opportunity to take more control over reducing their risk of heart disease in the future.’

The team are trying to establish whether adding flavonoids to the diet gives protection on top of that provided by prescription drugs.

What is other than clear is whether the 'protective effect' will actually arise from the regular eating of chocolate containing sugar and that that sugar could well be the heart protective factor ... protecting the heart against sudden Relative HYPOglycemia Distress [aka RHOD] which can cause the heart to stop because of lack of glucose/sugar fuel from the blood.

What controls will the study include, for example 'sugar free' chocolate, to help ascertain true 'cause & effect' in relation to glucose/sugar?

This is particularly important for the women who are the focus of this research, as deaths due to heart disease rise rapidly after the menopause and having type 2 diabetes, treated by glucose [blood sugar] lowering drugs, increases this risk a further three and a half times.

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Daily Mail
28 Apr 2008

EdBiew LIFE2345.cOM Every decisecond Better GroundHog-Day and Jonathan Livingston Seagulls LOVE explains why LOVE-diabetes and the CURE and ...HOW ?

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Insulin induced HYPOglycemia: comparison of glucose and glycerol concentrations in plasma and microdialysate from subcutaneous adipose tissue - Kamel

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Archives of Disease in Childhood

The journal of the Royal College of Paediatrics and Child Health.

1999 Jan;80(1):42-45

Links

Kamel A, Norgren S, Persson B, Marcus C.

Claude.Marcus@pediat.hs.sll.se

Department of Pediatrics, Huddinge University Hospital, Sweden.

AIMS: To investigate the dynamics between plasma and dialysate glucose during HYPOglycemia in children.

STUDY DESIGN: Six children in pre-puberty or early puberty were investigated by multiple blood sampling and micro-dialysis of subcutaneous adipose tissue during a standard arginine-insulin tolerance test.

Glucose and glycerol, as an index of lipolysis, were measured in samples from both compartments. Plasma concentrations of insulin and the main counter-regulatory hormones were also measured.

RESULTS: Plasma and dialysate glucose concentrations were very similar at baseline and increased in concert after infusion of arginine, probably in response to glucagon release.

After insulin injection, glucose in both plasma and dialysate fell in parallel. The subsequent Relative HYPOglycemia Distress [RHOD] response induced a rapid rebound in the plasma concentration with a mean (SD) delay in the dialysate of 16 (3) minutes.

Plasma glycerol was approximately five-fold lower than in the dialysate and did not fluctuate significantly.

Dialysate glycerol decreased with arginine infusion and reached a nadir immediately following insulin administration.

Subsequently, the anti-lipolytic effect of insulin was overcome by the Relative HYPOglycemia Distress [RHOD] response, and lipolysis prevailed in spite of HYPERinsulinemia.

CONCLUSION: Rapid insulin/Relative HYPOglycemia Distress [RHOD] induced rebound of interstitial glucose concentrations is significantly delayed compared with the extraordinarily rapid ... insulin/RHOD induced rebound of blood plasma glucose concentrations, and the anti-lipolytic effect of HYPERinsulinemia is opposed possibly by the glucagonic RHOD response.

Keywords: arginine; insulin; glucose; glycerol; lipolysis; catecholamines; microdialysis; hypoglycaemia

http://www.ncbi.nlm.nih.gov/pubmed/10325757

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

• Ungerstedt U. Microdialysis--principles and applications for studies in animals and man. J Intern Med. 1991 Oct;230(4):365–373. [PubMed]
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• Elimam A, Horal M, Bergström M, Marcus C. Diagnosis of hypoglycaemia: effects of blood sample handling and evaluation of a glucose photometer in the low glucose range. Acta Paediatr. 1997 May;86(5):474–478. [PubMed]
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• Bolinder J, Hagström E, Ungerstedt U, Arner P. Microdialysis of subcutaneous adipose tissue in vivo for continuous glucose monitoring in man. Scand J Clin Lab Invest. 1989 Sep;49(5):465–474. [PubMed]
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• Horal M, Ungerstedt U, Persson B, Westgren M, Marcus C. Metabolic adaptation in IUGR neonates determined with microdialysis--a pilot study. Early Hum Dev. 1995 May 12;42(1):1–14. [PubMed]
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• Hildingsson U, Selldén H, Ungerstedt U, Marcus C. Microdialysis for metabolic monitoring in neonates after surgery. Acta Paediatr. 1996 May;85(5):589–594. [PubMed]
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• Kamel A, Norgren S, Ehrén H, Hildingsson U, Marcus C. Antilipolytic effect of insulin and insulin receptor messenger RNA expression in adipocytes of infants, children, and adults. Pediatr Res. 1997 Apr;41(4 Pt 1):563–567. [PubMed]
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• Aynsley-Green A. Glucose: a fuel for thought! J Paediatr Child Health. 1991 Feb;27(1):21–30. [PubMed]
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• Marcus C, Karpe B, Bolme P, Sonnenfeld T, Arner P. Changes in catecholamine-induced lipolysis in isolated human fat cells during the first year of life. J Clin Invest. 1987 Jun;79(6):1812–1818. [PubMed]
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• Engfeldt P, Hellmér J, Wahrenberg H, Arner P. Effects of insulin on adrenoceptor binding and the rate of catecholamine-induced lipolysis in isolated human fat cells. J Biol Chem. 1988 Oct 25;263(30):15553–15560. [PubMed]
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• Bolinder J, Sjöberg S, Arner P. Stimulation of adipose tissue lipolysis following insulin-induced hypoglycaemia: evidence of increased beta-adrenoceptor-mediated lipolytic response in IDDM. Diabetologia. 1996 Jul;39(7):845–853. [PubMed]
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• Hagström-Toft E, Enoksson S, Moberg E, Bolinder J, Arner P. Absolute concentrations of glycerol and lactate in human skeletal muscle, adipose tissue, and blood. Am J Physiol. 1997 Sep;273(3 Pt 1):E584–E592. [PubMed]
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• Pugliese M, Lifshitz F, Fort P, Cervantes C, Recker B, Ginsberg L. Pituitary function assessment in short stature by a combined hormonal-stimulation test. Am J Dis Child. 1987 May;141(5):556–561. [PubMed]
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• Heding LG. Determination of total serum insulin (IRI) in insulin-treated diabetic patients. Diabetologia. 1972 Aug;8(4):260–266. [PubMed]
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• Hjemdahl P, Daleskog M, Kahan T. Determination of plasma catecholamines by high performance liquid chromatography with electrochemical detection: comparison with a radioenzymatic method. Life Sci. 1979 Jul 9;25(2):131–138. [PubMed]
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• Barham D, Trinder P. An improved colour reagent for the determination of blood glucose by the oxidase system. Analyst. 1972 Feb;97(151):142–145. [PubMed]
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• Foster KJ, Alberti KG, Hinks L, Lloyd B, Postle A, Smythe P, Turnell DC, Walton R. Blood intermediary metabolite and insulin concentrations after an overnight fast: reference ranges for adults, and interrelations. Clin Chem. 1978 Sep;24(9):1568–1572. [PubMed]
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• Bolinder J, Ungerstedt U, Arner P. Microdialysis measurement of the absolute glucose concentration in subcutaneous adipose tissue allowing glucose monitoring in diabetic patients. Diabetologia. 1992 Dec;35(12):1177–1180. [PubMed]
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• Bolinder J, Hagström-Toft E, Ungerstedt U, Arner P. Self-monitoring of blood glucose in type I diabetic patients: comparison with continuous microdialysis measurements of glucose in subcutaneous adipose tissue during ordinary life conditions. Diabetes Care. 1997 Jan;20(1):64–70. [PubMed]
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• Felländer G, Nordenström J, Ungerstedt U, Arner P, Bolinder J. Influence of operation on glucose metabolism and lipolysis in human adipose tissue: a microdialysis study. Eur J Surg. 1994 Feb;160(2):87–95. [PubMed]
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• Fernqvist-Forbes E, Linde B, Gunnarsson R. Insulin absorption and subcutaneous blood flow in normal subjects during insulin-induced hypoglycemia. J Clin Endocrinol Metab. 1988 Sep;67(3):619–623. [PubMed]
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• Jansson PA, Fowelin JP, von Schenck HP, Smith UP, Lönnroth PN. Measurement by microdialysis of the insulin concentration in subcutaneous interstitial fluid. Importance of the endothelial barrier for insulin. Diabetes. 1993 Oct;42(10):1469–1473. [PubMed]
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• Kahn BB, Flier JS. Regulation of glucose-transporter gene expression in vitro and in vivo. Diabetes Care. 1990 Jun;13(6):548–564. [PubMed]
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• Nyberg G, Häger A, Smith U. Effect of age on human adipose tissue metabolism and hormonal responsiveness. Acta Paediatr Scand. 1977 Jul;66(4):495–500. [PubMed]
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• Morris AA, Thekekara A, Wilks Z, Clayton PT, Leonard JV, Aynsley-Green A. Evaluation of fasts for investigating hypoglycaemia or suspected metabolic disease. Arch Dis Child. 1996 Aug;75(2):115–119. [PubMed]
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• Marcus C, Sonnenfeld T, Karpe B, Bolme P, Arner P. Inhibition of lipolysis by agents acting via adenylate cyclase in fat cells from infants and adults. Pediatr Res. 1989 Sep;26(3):255–259. [PubMed]
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• Marcus C, Selldén H, Rickardsson E, Lönnqvist PA, Brönnegård M, Arner P. Lack of lipolytic response in infants after endotracheal intubation. Arch Dis Child. 1993 Mar;68(3):402–404. [PubMed]
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• Marcus C, Ehrén H, Bolme P, Arner P. Regulation of lipolysis during the neonatal period. Importance of thyrotropin. J Clin Invest. 1988 Nov;82(5):1793–1797. [PubMed]

LIFE2345.cOM every decisecond choice ...HOW ?

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Brain insulin: regulation, mechanisms of action and functions.

Gerozissis K.

Chercheur INSERM, UMR 7059 CNRS, Paris Cedex, France. gerozissis@yahoo.co.uk

1. While many questions remained unanswered, it is now well documented that, contrary to earlier views, insulin is an important neuromodulator, contributing to neurobiological processes, in particular energy homeostasis and cognition. A specific role on cognitive functions related to feeding is proposed, and it is suggested that brain insulin from different sources might be involved in the above vital functions in health and disease.

2. A molecule identical to pancreatic insulin, and specific insulin receptors, are found widely distributed in the central nervous system networks related to feeding, reproduction, or cognition.

3. The actions of insulin in the central nervous system may be under both multilevel and multifactorial controls. The amount of blood insulin reaching the brain, brain insulin stores and secretion, potential local biosynthesis and degradation of the peptide, and insulin receptors and signal transduction can be affected by metabolic factors induced by nutrients, hormones, neurotransmitters, and regulatory peptides, peripherally or in the central nervous system.

4. Glucose and serotonin regulate insulin directly in the hypothalamus and may be of importance for its biological effects. Central mechanisms regulating glucose-induced insulin secretion show some analogy with the mechanisms operating in the pancreas.

5. A cross-talk between insulin and leptin receptors has been observed in the brain, and a regulation of central insulin actions, potentially via serotonin modulation, by leptin, galanin, melancortins, and neuropeptide Y (NPY) is suggested.

6. A more complete knowledge of the biological role of insulin in brain function and dysfunction, and of the regulatory mechanisms involved in these processes, constitutes a real advancement in the understanding of the pathophysiology of metabolic and mental diseases and could lead to important medical benefits.

http://www.ncbi.nlm.nih.gov/pubmed/12701881

Complete Freund's Adjuvant

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J Immunol. 1993 Mar 1;150(5):2072-80. Links

Complete Freund's Adjuvant aka CFA ... induced T cells ... apparently prevent the development and adoptive transfer of diabetes in non-obese diabetic mice.

Qin HY, Sadelain MW, Hitchon C, Lauzon J, Singh B.

Department of Immunology, University of Alberta, Edmonton, Canada.

T1 or Insulin-dependent diabetes mellitus is a condition of above average blood glucose concentration (AABGC) that is usually characterized by down-regulation of the quantity and/or mass of insulin-producing beta-cells in the islet of Langerhans of the pancreas.

The condition in non-obese diabetic (NOD) mice can be prevented by a single injection of CFA.

This study explores the cellular basis and the time course of the reduction in AABGC.

Since CFA contains a mycobacterial cell wall that has adjuvant property, the role of mycobacteria in young NOD mice was investigated.

Mice injected with Mycobacterium tuberculosis or Mycobacterium bovis (BCG vaccine) at 4 wk of age were also found to be prevented from developing AABGC.

It was found that prevention of AABGC is only achieved by administration of CFA between 4 and 10 wk of age.

Draining lymph node cells or spleen cells from CFA-treated NOD mice transfer the prevention of AABGC. Adoptive transfer of spleen cells from CFA-treated mice with spleen cells from acutely diabetic mice delayed the induction of any AABGC condition into irradiated recipient mice. CFA-treated old NOD mice were also resistant to passive transfer of any AABGC condition by spleen cells from acutely diabetic mice.

Depletion of the Thy 1.2+ cells or CD4(+)-bearing T cells abrogated the prevention of developing AABGC. However, diabetes can be induced in the 'treated' mice by cyclophosphamide treatment.

It was also found that thymocytes from NOD mice responded only weakly to mitogen Con A. CFA treatment, however, restored the ability of these cells to respond to Con A. Finally, the results apparently suggest that T cells induced after CFA treatment of NOD mice prevent both the induction & effector phases of the AABGC condition.

http://www.ncbi.nlm.nih.gov/pubmed/8436836

UNdrugTREATED rare but well defined ...HOW ?

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What is CFA ? ? ?

'Complete Freund's Adjuvant' is an antigen solution emulsified in mineral oil, used as an immunopotentiator (booster of the immune system).

Forms

The so-called complete form (CFA) is composed of inactivated and dried mycobacteria, usually Mycobacterium tuberculosis (the pathogenic agent of tuberculosis).

The so-called incomplete form (IFA) is the same adjuvant, but without the mycobacterial components.

Eponym

It is named after Jules T. Freund (1890-1960), Hungarian-born American immunologist.

Regulation

Freund's adjuvant is effective in stimulating cell-mediated immunity and may lead to the potentiation of the production of certain immunoglobulins, but this effect depends on the animal model used. Its use in humans is forbidden, due to its toxicity. Even for animal research there are currently guidelines associated with its use, due to its painful reaction and potential for tissue damage. Injections of CFA should be subcutaneous or intraperitoneal, because intradermal injections may cause skin ulceration and necrosis; intramuscular injections may lead to temporary or permanent muscle lesion, and intravenous injections may produce pulmonary lipid embolism.

Effects

When administered to mice, in some laboratory experiments Freund's complete adjuvant was said to have prevented juvenile-onset diabetes^[1][2] and combined with prepared spleen cells was said to have reversed it.^[3] In 2006 these claims were challenged by the findings of several other researchers.^[4] Although newspapers have described the 2006 findings as confirming the earlier experiments,^[5] in substantial ways they conflict with them. A report from NIH was released on November 23, 2006 in Science confirming the participation of spleen cells in reversing end-stage diabetes.^[6][7]

It has also been investigated in an animal model of Parkinson's disease.^[8]

Mechanism

The adjuvant is known to stimulate production of tumor necrosis factor, which is thought to kill the T-cells responsible for the autoimmune destruction of the pancreatic Beta cells. Still in question is whether the regrowth of functional insulin-producing cells occurs due to differentiation and proliferation of existing pancreatic stem cells, or whether the injected spleen cells re-differentiate to an insulin producing form. Denise Faustman, whose work has been central to developing the protocol, has suggested that both mechanisms may play a role. However, in experiments to verify and examine her work, Suri reported that DNA-based evidence yielded no sign of spleen cell derivatives in pancreatic islet Beta cells analyzed after treatments.^[9]

External links

• Recommendations for Use and Alternatives to Freund's Complete Adjuvant. University of Iowa

References

1. ^ Sadelain, M.W., et al. (1991), "Prevention of type I diabetes in NOD mice by adjuvant immunotherapy", Diabetes 39(5): 583-589, <http://diabetes.diabetesjournals.org/cgi/content/abstract/39/5/583>
2. ^ Qin, H.Y., et al. (1993), "Complete Freund’s adjuvant-induced T cells prevent the development and adoptive transfer of diabetes in nonobese diabetic mice", J. Immunol. 150: 2072–2080, <http://www.jimmunol.org/cgi/content/abstract/150/5/2072>
3. ^ Kodama, S., et al. (2003), "Islet Regeneration During the Reversal of Autoimmune Diabetes in NOD Mice", 'Science' 302: 1223-1227, <http://www.sciencemag.org/cgi/content/abstract/302/5648/1223>
4. ^ Couzin, J. (2006), "Diabetes Studies Conflict on Power of Spleen Cells", Science 311: 1694, <http://www.sciencemag.org/cgi/content/full/311/5768/1694>
5. ^ Kolata, G. (2006 March 25), "A Controversial Therapy for Diabetes Is Verified", New York Times, <http://www.nytimes.com/2006/03/24/health/24diabetes.html>
6. ^ New data from NIH lab confirms protocol to reverse type 1 diabetes in mice, BiologyNewsNet, November 2006
7. ^ Philip E. Ross, Putting Up with Self, Scientific American, November 12, 2006
8. ^ Armentero MT, Levandis G, Nappi G, Bazzini E, Blandini F (2006). "Peripheral inflammation and neuroprotection: systemic pretreatment with complete Freund's adjuvant reduces 6-hydroxydopamine toxicity in a rodent model of Parkinson's disease". Neurobiol. Dis. 24 (3): 492–505. doi:10.1016/j.nbd.2006.08.016. PMID 17023164.
9. ^ Suri, A., et al. (2006), "Immunological Reversal of Autoimmune Diabetes Without Hematopoietic Replacement of β Cells", Science 311: 1778-1780

Daily Mail, 24 Apr 2008. Page 13

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Daily Mail
24 Apr 2008

Think yourself thinner

Remembering meals cuts the appetite...

By David Derbyshire

IF you’re feeling hunger pangs but want to lose weight, try thinking yourself thinner.

British scientists have shown that actively remembering your last meal suppresses appetite and reduces the desire to snack on junk food.

They have also shown that concentrating on food while eating – rather than grabbing a meal in front of the TV – makes you less likely to get hungry later on.

The findings suggest that weight watchers can teach themselves to be less greedy – and that techniques such as hypnotism and behavioural therapy could help.

The findings come from Dr Suzanne Higgs and colleagues at the University of Birmingham who devised a series of experiments to test the impact of memory of food on snacking.

In one, 47 female students were told they were taking part in a biscuit taste test. They were given lunch then split into two groups.

Dr Higgs told half the students to write a detailed description of their lunch, while the rest were asked to describe their journey to the campus.

After the taste test – which had been designed to disguise the true nature of the experiment – the women were invited to eat their fill of the remaining biscuits.

Women who had been asked to write a description of their lunch – making the memory of it vivid in their minds – ate far fewer biscuits than those who had been asked to describe their journey to work, New Scientist reports today.

The memory effect was small among women who took the test one hour after eating. But it became more powerful as the day drew on. Three hours after lunch, women who had been asked to describe their meal had a ‘significantly reduced appetite’ compared with those who did not.

In other experiments, a video was played to some of the women during the lunch to distract them. Those who were watching the video – and not concentrating on their food – tended to snack more later in the day. This suggests that actively concentrating on meals – rather than grabbing food in front of the television – could reduce appetite later in the day.

The part of the brain involved in remembering recent meals is the hippocampus. The findings raise the possibility that drugs designed to boost activity in the hippocampus could suppress appetite.

Other studies have shown that those with damage to the hippocampus can lose their restraint when it comes to eating.

Dr Paul Rozin, of the University of Pennsylvania, Philadelphia, said: ‘Such folks will eat second and third lunches, so it makes some sense that activating the hippocampus might inhibit eating.’