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Pesticides ‘linked to Parkinson’s’

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Pesticides ‘linked to Parkinson’s’

A pesticide is a substance or mixture of substances used to kill a pest.[1] A pesticide is any substance or mixture of substance intended for: – preventing, destroying, repelling or mitigating any pest.[2] A pesticide may be a chemical substance, biological agent (such as a virus or bacteria), antimicrobial, disinfectant or device used against any pest. Pests include insects, plant pathogens, weeds, molluscs, birds, mammals, fish, nematodes (roundworms), microbes and people that destroy property, spread or are a vector for disease or cause a nuisance. Although there are benefits to the use of pesticides, there are also drawbacks, such as potential toxicity to humans and other animals.

2,4-Dichlorophenoxyacetic acid – known as 2,4-D – used to kill a range of weeds

Permethrin – used in pest control, including ant powder and flea killer. Sprayed on tents and nets to repel mosquitoes

Paraquat – weedkiller used on a range of crops including potatoes. Banned for use in Europe since 2007

Dieldrin – pesticide, banned for use in Europe

Diquat – general weedkiller

Maneb – kills fungus, used to protect potatoes, tomatoes and other crops

Mancozeb – also kills fungus, used to protect potatoes among other crops

Rotenone – used to eradicate unwanted fish species as well as other pests

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Lifestyle affects risk of second breast cancer

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Lifestyle affects risk of second breast cancer

Surviving breast cancer is no guarantee that a new cancer won’t appear in the other breast. However, research now suggests that women can build their own personal armor to at least partially protect themselves from this occurring.

All it takes, says Dr. Christopher I. Li, is to “stay at a normal weight, don’t smoke, and drink in moderation.”

The research, headed up by Li at the Fred Hutchinson Cancer Center in Seattle, Washington, suggests that obesity, smoking and drinking too much are all risk factors for breast cancer in the opposite breast — also called the “contralateral” breast — of women who’ve had an “estrogen receptor-positive invasive breast cancer.”

That’s because estrogen can fuel these tumors’ growth, and both fat tissue and excessive alcohol use directly increase estrogen levels in the body, Li and his team propose. They believe that smoking contributes to the risk because of all the cancer-causing substances one inhales when smoking.

Until now, there haven’t been many studies regarding ways that women could protect themselves from second breast cancers, according to the report in the September 8th online issue of the Journal of Clinical Oncology.

The new study included 365 women with a first estrogen receptor-positive breast cancer and a second contralateral cancer and 726 control subjects. By reviewing medical charts and interviewing the women directly, the researchers determined body mass index (BMI) and alcohol and tobacco use. BMI is an estimate of a person’s relative body fat calculated from her height and weight.

Compared with normal weight women, those who were obese were almost half again – by 40% — as likely to develop a contralateral breast cancer. Consumption of 7 or more alcoholic drinks per week nearly doubled the risk compared with no alcohol use. Findings were similar for current smoking.

Women who both smoke and drink following diagnosis of the first cancer had an even greater risk of a second cancer. The study showed that consuming 7 or more alcoholic drinks per week coupled with current smoking increased the odds of contralateral breast cancer more than 7-fold.

In a related editorial, Dr. Jennifer A. Ligibel, from the Dana-Farber Cancer Institute in Boston, points out that the study by Li and his team took place before use of hormonal therapy for estrogen receptor-positive breast cancer became routine. Therefore, a more modern study examining the effect of modifiable lifestyle factors should involve patients treated according to current guidelines.

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Junk food makes you eat more

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Junk food makes you eat more

It triggers messages that are sent to the body’s cells, warning them to ignore appetite-suppressing hormones that regulate our weight.

The effect can last for a few days sabotaging efforts to get back to a healthy diet afterwards, the study found.

The study shows for the first time how particular products can create a vicious cycle of food bingeing.

Lead author Dr Deborah Clegg of the study by UT Southwestern Medical Centre in Dallas, said: “Normally, our body is primed to say when we have had enough, but that does not always happen when we are eating something good.

“What we have shown is that someone’s entire brain chemistry can change in a very short period of time.

“Our findings suggest that when you eat something high in fat, your brain gets ‘hit’ with the fatty acids, and you become resistant to insulin and leptin. Since you are not being told by the brain to stop eating, you overeat.”

The hormone leptin is produced in the brain and suppresses hunger while insulin is produced by the pancreas and regulates blood sugar levels.

Although the study was performed on rats and mice the scientists said their results reinforced common dietary recommendations to limit saturated fat intake as “it causes you to eat more.”

The animals received the same amount of calories in one of three forms of fat – palmitic acid, monounsaturated fatty acid or unsaturated oleic acid which is found in olive and grapeseed oils.

The biggest affect on leptin and insulin was caused by molecules from palmitic acid which is found in beef, butter, cheese and milk.

Dr Clegg, whose findings are published in The Journal of Clinical Investigation, said: “The action was very specific to palmitic acid, which is very high in foods that are rich in saturated fat.

She said it may explain why many people who overindulge on a Friday or Saturday say they are hungrier than normal on Monday.

The findings may also have implications for diabetes research because although scientists have known a high-fat diet can cause insulin resistance, little has been known about the mechanism behind it or whether specific types of fat are more dangerous.

Dr Clegg said: “We found the palmitic acid specifically reduced the ability of leptin and insulin to activate their intracellular signalling cascades. The oleic fat did not do this.”

She said the other key finding is this mechanism is triggered in the brain – long before there might be signs of obesity anywhere else in the body.

Dr Clegg said the next step is to determine how long it takes to reverse completely the effects of short-term exposure to high-fat food.

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