[alan aragon]

Not a nutrition topic, but I thought it was interesting & related to what we're discussing:

Abstract
Objectives: There is concern regarding the possible health effects of cellular telephone use. We examined whether the source of funding of studies of the effects of low-level radiofrequency radiation is associated with the results of studies. We conducted a systematic review of studies of controlled exposure to radiofrequency radiation with health-related outcomes (electroencephalogram, cognitive or cardiovascular function, hormone levels, symptoms, and subjective well-being) .

Data sources: We searched EMBASE, Medline, and a specialist database in February 2005 and scrutinized reference lists from relevant publications.

Data extraction: Data on the source of funding, study design, methodologic quality, and other study characteristics were extracted. The primary outcome was the reporting of at least one statistically significant association between the exposure and a health-related outcome. Data were analyzed using logistic regression models.

Data synthesis: Of 59 studies, 12 (20%) were funded exclusively by the telecommunications industry, 11 (19%) were funded by public agencies or charities, 14 (24%) had mixed funding (including industry) , and in 22 (37%) the source of funding was not reported. Studies funded exclusively by industry reported the largest number of outcomes, but were least likely to report a statistically significant result: The odds ratio was 0.11 (95% confidence interval, 0.02–0.78) , compared with studies funded by public agencies or charities. This finding was not materially altered in analyses adjusted for the number of outcomes reported, study quality, and other factors.

Conclusions: The interpretation of results from studies of health effects of radiofrequency radiation should take sponsorship into account.

http://www.ehponline.org/docs/2006/9149/abstract.html

[EasyEJL]

The money is definitely an issue. Its so hard though as at the same time I hate the government funding studies too

[alan aragon]

More reasons to pay attention to funding source, here's a drug industry systematic review:

http://www.bmj.com/cgi/content/full/326/7400/1167

Discussion

Research sponsored by the drug industry was more likely to produce results favouring the product made by the company sponsoring the research than studies funded by other sources. The results apply across a wide range of disease states, drugs, and drug classes, over at least two decades and regardless of the type of research being assessed—pharmacoeconomic studies, clinical trials, or meta-analyses of clinical trials. The totality of the evidence reported in our meta-analysis of a subset of homogeneous studies suggests that there is some kind of systematic bias to the outcome of published research funded by the pharmaceutical industry.
Our results confirm and extend those reported by Bekelman et al.8 They identified only five studies that compared outcomes in research funded by pharmaceutical companies and other sources,14 16 20 23 41 and our study adds another 16 studies12 13 15 18 19 22 24 26 27 30 32 34 36 38–40 Our results are also supported by Rochon and coworkers43 (we excluded this paper because all of the trials were sponsored by drug companies and were, therefore, not comparible with trials lacking company funding.) They found that trials supported by manufacturers of non-steroidal anti-inflammatory agents almost always reported that the sponsor's drug was as or more effective and less toxic than the comparison drug.

Explanations

At least four possible explanations exist for favourable results seen in industry sponsored research. Firstly, pharmaceutical companies may selectively fund trials on drugs that they consider to be superior to the competition. Data collected so far, however, indicate that researchers cannot predict results of trials in advance.44

Secondly, positive results could be the consequence of poor quality research conducted by industry. For example, low quality trials exaggerate the benefits of treatment by an average of 34%.45 46 We found that the research methods of trials sponsored by drug companies is at least as good as that of non-industry funded research and in many cases better. This does not guarantee the absence of bias in studies sponsored by the industry since outcome could be influenced by factors left out of quality scores, such as the question asked or the conduct or reporting of the study.7 47

Thirdly, selecting an appropriate comparator is a key issue in planning a clinical trial.7 20 44 In the study by Rochon et al, in most cases in which the doses of the study and comparator drugs were not equivalent, the drug given at the higher dose was that of the supporting manufacturer.43 As the authors saw, higher doses may bias the results in favour of effectiveness of the manufacturer's product. Safer also reports that in trials of psychiatric drugs the comparator drug is often given in doses outside the usual range or there is a rapid and substantial dose increase in the drug not manufactured by the sponsoring company.48 In another instance, research funded by the company marketing fluconazole compared it with oral amphotericin B, a drug known to be poorly absorbed, thereby creating a bias in favour of fluconazole.49 We did not consider who is finally responsible for the selection of the comparator—investigators, regulatory agencies, or sponsors.

Finally, our results suggest that publication bias may explain our finding of bias in favour of outcomes of research funded by industry. Although research sponsored by industry was less likely to be published than research with other sources of funding, the two studies with this finding did not specifically examine whether non-publication applied just to research with non-significant outcomes.17 21 In the past few years, manufacturers have attempted to prevent studies which are unfavourable to their products from being published in several high profile cases.50–52

[bioman]

The cell phone EMR thingy is going to be a huge issue in the next 5 years.

[MrBrightside]

Would this potentially conflict with products like Palo Alto's Leviathan, whose product's most effective when insulin levels are lower? It seems to me like it'd be impossible to take Leviathan if you're mega-dosing.

[EasyEJL]

hmm what would make you think that fish oil rasises insulin levels round the clock? If anything I would think it lowers it.

[MrBrightside]

It looks like I mistook insulin sensitivity to mean heightened insulin levels, but I swear I saw somewhere that it raised insulin levels.

The insulin sensitivity would not interfere with anything that depends on lower insulin levels then, right?

[Force of Green]

Originally Posted by MrBrightside

It looks like I mistook insulin sensitivity to mean heightened insulin levels, but I swear I saw somewhere that it raised insulin levels.

The insulin sensitivity would not interfere with anything that depends on lower insulin levels then, right?

Watch yourself MrBrightside. You're walking on thin ice.

[EasyEJL]

hard to say for sure without using blood glucose testers. It doesn't seem to do any harm or reduction of usefulness to them

[datBtrue]

Originally Posted by MrBrightside

It looks like I mistook insulin sensitivity to mean heightened insulin levels, but I swear I saw somewhere that it raised insulin levels.

The insulin sensitivity would not interfere with anything that depends on lower insulin levels then, right?

Don't be silly. You can find all the scientific information you want in a thread I posted a while back that includes lengthy sections from two books: Evolutionary Aspects of Diet, the Omega-6/Omega-3 Ratio, and Gene Expression

From the second book Novel food ingredients for weight control, C.J.K. Henry (Editor), CRC; 1 edition (May 11, 2007) you'll find plenty of information to answer your questions including:

13.3.4 The mechanism of polyunsaturated fatty acid in insulin resistance and type 2 diabetes

The molecular effects of PUFAs are such that these fatty acids may have an impact on the regulation of insulin sensitivity (Lombardo and Chicco, 2006). There are indeed indications that omega-3 PUFAs may have positive effects on glucose tolerance by reducing insulin resistance, as demonstrated in rodent models of obesity (Storlien et al., 2000). Rats fed a high-fat diet supplemented with a low ratio of omega-6: omega-3 PUFA maintained normal insulin action, while rats fed a diet containing high levels of saturated and monounsaturated fats showed insulin resistance in several tissues (Storlien et al., 1991). Feeding fish oil to mice, providing 5–10% of the daily energy intake, accelerated glucose uptake and maintained glucose homeostasis during high-fat feeding (Storlien et al., 1997). The favourable effects of fish oil-derived PUFAs may be explained by suppression of hepatic fatty acids synthesis and increased fat oxidation. Another mechanism behind the positive effects of PUFAs on insulin sensitivity may occur through alteration in the plasma membrane composition of the cells. There is some evidence indicating that altered membrane structure may affect both insulin action and insulin binding to its receptor (Storlien et al., 1996). Another possible mechanism behind the effects of PUFAs in metabolism can be attributed to changes in protein acylation. Many membrane proteins are modified by fatty acid acylation with saturated fatty acids like palmitate or myristate. Whether this has any significant effects in insulin signalling, or whether PUFAs play a role, is unknown at the present time. In summary, the metabolic effects of omega-3 PUFAs promote the reduction of triglyceride in skeletal muscle and liver, which in turn is associated with improved insulin action and glucose tolerance thereby preventing development of insulin resistance.

Furthermore,

13.3.5 Islet metabolism, insulin secretion and polyunsaturated fatty acid

Besides insulin resistance defective islet function is also of importance for the development of glucose intolerance and type 2 diabetes. In fact, a normal islet function with a normal compensation in insulin secretion is a prerequisite for maintaining normal glucose homeostasis in insulin resistance (Ahren and Pacini, 2005). Therefore, to improve glucose homeostasis, effects on islet function are required. Fatty acids are known to acutely stimulate insulin secretion via several possible pathways. First, it is believed that fatty acids are taken up into the B-cell, where they are converted to long-chain acyl-CoA (LC-CoA). Through glucose metabolism the uptake and oxidation of the fatty acids are blocked through the effect of malonyl- CoA, which accumulates in the cytosol when B-cells are exposed to high glucose concentrations (Corkey et al., 1989, Prentki et al., 1992). Malonyl- CoA is an effective inhibitor of CPT-1, inhibiting the transport of fatty acyl-CoA into the mitochondria, resulting in increased accumulation of LC-CoA in the cytosol. LC-CoA has been found to exert effects at several levels in the B-cell to promote second-phase insulin secretion: through binding to the KATP channels, affecting the exocytosis of insulin granulae, activation of protein kinases via acylation mechanism and thereby promoting insulin secretion (Corkey et al., 2000, Deeney et al., 2000, Yaney et al., 2000). Although this seems to be a common pathway for most of the fatty acids, saturated fats are more potent in stimulating glucose-induced insulin secretion than unsaturated ones, as was recently observed in isolated human islets (Gravena et al., 2002).

Another pathway for the fatty acids to stimulate insulin secretion is through the fatty acid binding protein GPR40 (Itoh et al., 2003; Salehi et al., 2005; Shapiro et al., 2005). This is a G-protein-coupled receptor that has fatty acids as substrate. Both saturated (C12–C16) and unsaturated (C18–C22) fatty acids have the potency to induce increased intracellular Ca2+ in Chinese hamster ovary (CHO) cells transfected with the GPR40 receptor (Itoh et al., 2003; Itoh and Hinuma, 2005). A third indirect pathway for fatty acids to stimulate insulin secretion is through phospholipase A2 (PLA2), which is activated during glucose stimulation (Simonsson and Ahren, 2000). PLA2 stimulates the formation of arachidonic acid and inhibition of PLA2 results in blunted arachidonic acid formation, which was accompanied by reduced glucose-stimulated insulin secretion. Fish oil has been found to induce insulin secretion through incorporation of the omega-3 PUFAs in the plasma membrane to compete with the production of arachidonic acid.

In a recent study, inclusion of 7% omega-3 PUFAs in a high-fat diet fed to rats resulted in lower glucose-stimulated insulin secretion from isolated islets, possibly through direct effects of the fatty acids on the islets, blocking the hyper-secretion induced by saturated fatty acids (Holness et al., 2003). In addition, in vivo, PUFA supplementation in rats fed a high-fat diet resulted in reversed insulin hyper-secretion, suggesting that PUFAs may have acute effects on islets resulting in reduced insulin secretion (Holness et al., 2004). Therefore, PUFAs seems to be protective at low doses in fatty acid-induced apoptosis and may have anti-apoptotic effects in islets in vivo. Furthermore, the normalising effect of omega-3 PUFAs on high-fat diet- induced hyperinsulinaemia in response to glucose may have long-term beneficial effects on insulin sensitivity.

[porkhide]

Originally Posted by Zombie

i was going to ask you about this. im not taking big doses of Fish oil , but since i runned out of cycle support i increased my dose from 6 gr ED to 9.6-12 gr and i have noticed that my blood got a nice bright red color and it takes longer to coagulate and to form scabs and once the scabs are formed they can be easyly removed. i got a nose bleed 3 days ago and it hasnt healed completely. it starts healing and eveything but if i sneeze i start with the nose bleed and it takes time to heal again. i think im going to drop the fish oil a few days till my nose bleeds stop.

Try adding spinach or vit K
helps wth clotting

[LoveMeSexy]

Would mega dosed fish oil be suitable for people susceptible to toxins like mercury i.e. people suffering from autism? Also would krill oil be the only safe fish oil for such a person and any ideas when the price of krill oil is going to come down to a reasonable price level?