Low vitamin D levels linked to diabetes risk

NEW YORK — Lower levels of vitamin D circulating in the bloodstream are tied to a higher risk of developing diabetes in a new study of Australian adults.

After following more than 5,000 people for 5 years, the researchers found those with lower than average vitamin D levels had a 57 percent increased risk of developing type 2 diabetes compared with people with levels in the recommended range.

"Studies like ours have suggested that blood levels of vitamin D higher than what is recommended for bone health may be necessary to reduce the risk of developing type 2 diabetes," said lead author Dr. Claudia Gagnon, a fellow at the Western Hospital at the University of Melbourne in Australia, where the study was done.

Vitamin D is manufactured by the body in response to sunlight and also occurs naturally in some foods, like eggs, cod and salmon. The vitamin is best known for its role in working with calcium to build bones.

The Institute of Medicine recommends that adults get about 600 IU of vitamin D a day to maintain circulating levels in the desirable range.

Past studies have shown that vitamin D may also help keep blood sugar levels under control. In type 2 diabetes, the most common form of the disease, the body can't use insulin it produces efficiently to control blood sugar levels. Vitamin D may play a role by increasing the release of insulin, Gagnon said.

To see whether circulating D levels and calcium consumption influenced insulin sensitivity and diabetes risk, Gagnon's team measured the vitamin D blood levels of 5,200 people without diabetes. After 5 years, about 200 of them had developed diabetes, and the researchers measured everyone's vitamin D levels again.

Risk of diabetes rises 57 percent
The researchers found that twice as many people — 6 in 100 — with low blood levels of vitamin D later developed diabetes, compared to those with blood levels in the normal range —3 in 100.

When the researchers took into consideration risk factors for diabetes such as age, waist circumference, and a family history of the disease, the increased risk from low D levels translated to 57 percent, relative to those with higher levels.

Calcium is also thought to participate in insulin release, but the researchers found no link between the mineral and risk of developing diabetes later.

"Lower levels of vitamin D in the blood were associated with an increased risk of developing type 2 diabetes," Gagnon told Reuters Health by e-mail. "However, our findings do not prove cause and effect."

Further studies are needed, Gagnon's group writes in the journal Diabetes Care, both to directly test whether vitamin D supplements make a difference in diabetes risk, and if so, to determine the optimal circulating D levels to minimize that risk.

It's hard to know what exactly the link between vitamin D and diabetes is, Dr. Ian de Boer, assistant professor of medicine at the University of Washington in Seattle, told Reuters Health.

Obesity, inactivity may be factors
But obesity and inactivity, the highest risk factors for type 2 diabetes, may be the cause of low vitamin D levels, said de Boer, who did not work on the Australian study.

Vitamin D has also been linked to lower risks of asthma, heart disease, and certain cancers. However, there hasn't been much evidence showing that taking supplements helps these conditions.

Vitamin D is widely available for less than $10 for a 2-month supply.

The sun is the major vitamin D source for most people, but salmon and fortified dairy products also contain a lot, de Boer added.

The best ways to reduce diabetes risk are still to exercise and eat a healthy diet, he said.

"I don't think there's conclusive information that supplementing with vitamin D reduces diabetes risk," de Boer said.

NEW YORK — Lower levels of vitamin D circulating in the bloodstream are tied to a higher risk of developing diabetes in a new study of Australian adults.

After following more than 5,000 people for 5 years, the researchers found those with lower than average vitamin D levels had a 57 percent increased risk of developing type 2 diabetes compared with people with levels in the recommended range.

"Studies like ours have suggested that blood levels of vitamin D higher than what is recommended for bone health may be necessary to reduce the risk of developing type 2 diabetes," said lead author Dr. Claudia Gagnon, a fellow at the Western Hospital at the University of Melbourne in Australia, where the study was done.

Vitamin D is manufactured by the body in response to sunlight and also occurs naturally in some foods, like eggs, cod and salmon. The vitamin is best known for its role in working with calcium to build bones.

The Institute of Medicine recommends that adults get about 600 IU of vitamin D a day to maintain circulating levels in the desirable range.

Past studies have shown that vitamin D may also help keep blood sugar levels under control. In type 2 diabetes, the most common form of the disease, the body can't use insulin it produces efficiently to control blood sugar levels. Vitamin D may play a role by increasing the release of insulin, Gagnon said.

To see whether circulating D levels and calcium consumption influenced insulin sensitivity and diabetes risk, Gagnon's team measured the vitamin D blood levels of 5,200 people without diabetes. After 5 years, about 200 of them had developed diabetes, and the researchers measured everyone's vitamin D levels again.

Risk of diabetes rises 57 percent
The researchers found that twice as many people — 6 in 100 — with low blood levels of vitamin D later developed diabetes, compared to those with blood levels in the normal range —3 in 100.

When the researchers took into consideration risk factors for diabetes such as age, waist circumference, and a family history of the disease, the increased risk from low D levels translated to 57 percent, relative to those with higher levels.

Calcium is also thought to participate in insulin release, but the researchers found no link between the mineral and risk of developing diabetes later.

"Lower levels of vitamin D in the blood were associated with an increased risk of developing type 2 diabetes," Gagnon told Reuters Health by e-mail. "However, our findings do not prove cause and effect."

Further studies are needed, Gagnon's group writes in the journal Diabetes Care, both to directly test whether vitamin D supplements make a difference in diabetes risk, and if so, to determine the optimal circulating D levels to minimize that risk.

It's hard to know what exactly the link between vitamin D and diabetes is, Dr. Ian de Boer, assistant professor of medicine at the University of Washington in Seattle, told Reuters Health.

Obesity, inactivity may be factors
But obesity and inactivity, the highest risk factors for type 2 diabetes, may be the cause of low vitamin D levels, said de Boer, who did not work on the Australian study.

Vitamin D has also been linked to lower risks of asthma, heart disease, and certain cancers. However, there hasn't been much evidence showing that taking supplements helps these conditions.

Vitamin D is widely available for less than $10 for a 2-month supply.

The sun is the major vitamin D source for most people, but salmon and fortified dairy products also contain a lot, de Boer added.

The best ways to reduce diabetes risk are still to exercise and eat a healthy diet, he said.

"I don't think there's conclusive information that supplementing with vitamin D reduces diabetes risk," de Boer said.

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Popular Drink Increases Stroke Risk

In a study of 2564 people of varying ethnic backgrounds, researchers at Columbia University in New York and the Miller School of Medicine in Miami found a significant correlation between diet soda consumption and the risk of stroke.

Begun in 1993, the Northern Manhattan Study known as NOMAS has been ongoing and still continues. Researchers divided people into seven groups: those who drank less than one soda of any type per month, those with moderate soda consumption (up to six per week), daily regular soda consumption (one or more daily), moderate diet soda only, daily diet soda only, moderate diet soda and sometimes regular soda, and daily diet soda with any regular soda consumption.

Scientists factored in the age, ethnicity, gender, exercise habits, smoking status, alcohol consumption, and caloric intake. During the test period participants had 559 strokes combined.

After considering all the other factors studied, researchers concluded that regular diet soda drinkers had a 48% increased chance of having a stroke, while those who drank diet soda every day had a 61% increased risk of stroke over those who drank other types of soda.

Concurrently, it is important to note that Diet Coke recently moved into the number two position of most popular beverage among Americans–a scary proposition considering the recent study findings.

The stroke culprit is likely aspartame, an artificial sweetener that has been linked to dozens of other health conditions. According to Lynne Melcombe, author of Health Hazards of White Sugar, research links aspartame to the following health conditions: anxiety attacks; appetite problems such as binge-eating and sugar cravings; birth defects; blindness and vision problems such as blurred vision, bright flashes, and tunnel vision; brain tumors; chest pain; depression and emotional problems; dizziness and vertigo; edema; epilepsy and seizures; fatigue; headaches and migraines; hearing loss and tinnitus; heart palpitations and arrhythmia; hyperactivity; insomnia; joint pain; learning disabilities; memory loss; menstrual irregularities and PMS (premenstrual syndrome); muscle cramps; nausea; numbness of extremities; psychiatric disorders; reproductive problems; skin lesions; slurred speech; and uterine tumors. Research even links aspartame to death. Aspartame’s effects can be mistaken for Alzheimer’s disease, chronic fatigue syndrome, epilepsy, Epstein-Barr virus, Huntington’s chorea, hypothyroidism, Lou Gehrig’s disease; Lyme disease, Ménière’s disease, multiple sclerosis, and postpolio syndrome.

According to Randall Fitzgerald, author of The Hundred-Year Lie, some of the cancers linked to aspartame include: brain, liver, lung, kidney, and lymphoreticular cancer.

In a study of 2564 people of varying ethnic backgrounds, researchers at Columbia University in New York and the Miller School of Medicine in Miami found a significant correlation between diet soda consumption and the risk of stroke.

Begun in 1993, the Northern Manhattan Study known as NOMAS has been ongoing and still continues. Researchers divided people into seven groups: those who drank less than one soda of any type per month, those with moderate soda consumption (up to six per week), daily regular soda consumption (one or more daily), moderate diet soda only, daily diet soda only, moderate diet soda and sometimes regular soda, and daily diet soda with any regular soda consumption.

Scientists factored in the age, ethnicity, gender, exercise habits, smoking status, alcohol consumption, and caloric intake. During the test period participants had 559 strokes combined.

After considering all the other factors studied, researchers concluded that regular diet soda drinkers had a 48% increased chance of having a stroke, while those who drank diet soda every day had a 61% increased risk of stroke over those who drank other types of soda.

Concurrently, it is important to note that Diet Coke recently moved into the number two position of most popular beverage among Americans–a scary proposition considering the recent study findings.

The stroke culprit is likely aspartame, an artificial sweetener that has been linked to dozens of other health conditions. According to Lynne Melcombe, author of Health Hazards of White Sugar, research links aspartame to the following health conditions: anxiety attacks; appetite problems such as binge-eating and sugar cravings; birth defects; blindness and vision problems such as blurred vision, bright flashes, and tunnel vision; brain tumors; chest pain; depression and emotional problems; dizziness and vertigo; edema; epilepsy and seizures; fatigue; headaches and migraines; hearing loss and tinnitus; heart palpitations and arrhythmia; hyperactivity; insomnia; joint pain; learning disabilities; memory loss; menstrual irregularities and PMS (premenstrual syndrome); muscle cramps; nausea; numbness of extremities; psychiatric disorders; reproductive problems; skin lesions; slurred speech; and uterine tumors. Research even links aspartame to death. Aspartame’s effects can be mistaken for Alzheimer’s disease, chronic fatigue syndrome, epilepsy, Epstein-Barr virus, Huntington’s chorea, hypothyroidism, Lou Gehrig’s disease; Lyme disease, Ménière’s disease, multiple sclerosis, and postpolio syndrome.

According to Randall Fitzgerald, author of The Hundred-Year Lie, some of the cancers linked to aspartame include: brain, liver, lung, kidney, and lymphoreticular cancer.

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FeLV and Feline Lymphoma

Weiss ATA, Klopfleisch R, Gruber AD: Prevalence of feline leukaemia provirus DNA in feline lymphomas, Journal of Feline Medicine & Surgery 12: 929, 2010.

Feline leukemia virus (FeLV) is an important pathogen of cats. Since development of screening assays and vaccines for FeLV, the prevalence of persistently infected cats has decreased. Recent studies have shown that the FeLV genetic material remains in cats exposed to the virus, though viral replication may not occur. Concern exists that this persistent viral DNA may contribute to development of lymphoma in cats. To determine if an association exists, samples from 50 cases of lymphoma were tested for the presence of FeLV. Viral DNA was detected in a high percentage of all types of feline lymphomas by these investigators. Thus, though the prevalence of FeLV infection as well as lymphoma has decreased with the development of control measures for FeLV, a significant portion of feline lymphomas appear to involve FeLV genetic material. [MK]

Related articles:

Stutzer B, Simon K, Lutz H et al: Incidence of persistent viraemia and latent feline leukaemia virus infection in cats with lymphoma, Journal of Feline Medicine & Surgery 13: 81, 2011.

More on cat health: Winn Feline Foundation Library

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Weiss ATA, Klopfleisch R, Gruber AD: Prevalence of feline leukaemia provirus DNA in feline lymphomas, Journal of Feline Medicine & Surgery 12: 929, 2010.

Feline leukemia virus (FeLV) is an important pathogen of cats. Since development of screening assays and vaccines for FeLV, the prevalence of persistently infected cats has decreased. Recent studies have shown that the FeLV genetic material remains in cats exposed to the virus, though viral replication may not occur. Concern exists that this persistent viral DNA may contribute to development of lymphoma in cats. To determine if an association exists, samples from 50 cases of lymphoma were tested for the presence of FeLV. Viral DNA was detected in a high percentage of all types of feline lymphomas by these investigators. Thus, though the prevalence of FeLV infection as well as lymphoma has decreased with the development of control measures for FeLV, a significant portion of feline lymphomas appear to involve FeLV genetic material. [MK]

Related articles:

Stutzer B, Simon K, Lutz H et al: Incidence of persistent viraemia and latent feline leukaemia virus infection in cats with lymphoma, Journal of Feline Medicine & Surgery 13: 81, 2011.

More on cat health: Winn Feline Foundation Library

Join us on Facebook

Follow us on Twitter

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Bacterial Ecosystems Divide People Into 3 Groups, Scientists Say

Correction Appended
In the early 1900s, scientists discovered that each person belonged to one of four blood types. Now they have discovered a new way to classify humanity: by bacteria. Each human being is host to thousands of different species of microbes. Yet a group of scientists now report just three distinct ecosystems in the guts of people they have studied.

Blood type, meet bug type.

“It’s an important advance,” said Rob Knight, a biologist at the University of Colorado, who was not involved in the research. “It’s the first indication that human gut ecosystems may fall into distinct types.”

The researchers, led by Peer Bork of the European Molecular Biology Laboratory in Heidelberg, Germany, found no link between what they called enterotypes and the ethnic background of the European, American and Japanese subjects they studied.

Nor could they find a connection to sex, weight, health or age. They are now exploring other explanations. One possibility is that the guts, or intestines, of infants are randomly colonized by different pioneering species of microbes.

The microbes alter the gut so that only certain species can follow them.

Whatever the cause of the different enterotypes, they may end up having discrete effects on people’s health. Gut microbes aid in food digestion and synthesize vitamins, using enzymes our own cells cannot make.

Dr. Bork and his colleagues have found that each of the types makes a unique balance of these enzymes. Enterotype 1 produces more enzymes for making vitamin B7 (also known as biotin), for example, and Enterotype 2 more enzymes for vitamin B1 (thiamine).

The discovery of the blood types A, B, AB and O had a major effect on how doctors practice medicine. They could limit the chances that a patient’s body would reject a blood transfusion by making sure the donated blood was of a matching type. The discovery of enterotypes could someday lead to medical applications of its own, but they would be far down the road.

“Some things are pretty obvious already,” Dr. Bork said. Doctors might be able to tailor diets or drug prescriptions to suit people’s enterotypes, for example.

Or, he speculated, doctors might be able to use enterotypes to find alternatives to antibiotics, which are becoming increasingly ineffective. Instead of trying to wipe out disease-causing bacteria that have disrupted the ecological balance of the gut, they could try to provide reinforcements for the good bacteria. “You’d try to restore the type you had before,” he said.

Dr. Bork notes that more testing is necessary. Researchers will need to search for enterotypes in people from African, Chinese and other ethnic origins. He also notes that so far, all the subjects come from industrial nations, and thus eat similar foods. “This is a shortcoming,” he said. “We don’t have remote villages.”

The discovery of enterotypes follows on years of work mapping the diversity of microbes in the human body — the human microbiome, as it is known. The difficulty of the task has been staggering. Each person shelters about 100 trillion microbes.

(For comparison, the human body is made up of only around 10 trillion cells.) But scientists cannot rear a vast majority of these bacteria in their labs to identify them and learn their characteristics.

As genetics developed, scientists learned how to study the microbiome by analyzing its DNA. Scientists extracted DNA fragments from people’s skin, saliva and stool. They learned how to recognize and discard human DNA, so that they were left with genes from the microbiome. They searched through the remaining DNA for all the variants of a specific gene and compared them with known species. In some cases, the variants proved to be from familiar bacteria, like E. coli. In other cases, the gene belonged to a species new to science.

These studies offered glimpses of a diversity akin to a rain forest’s. Different regions of the body were home to different combinations of species. From one person to another, scientists found more tremendous variety. Many of the species that lived in one person’s mouth, for example, were missing from another’s.

Scientists wondered if deeper studies would reveal a unity to human microbiomes. Over the past few years, researchers have identified the genomes — the complete catalog of genes — of hundreds of microbe species that live in humans. Now they can compare any gene they find with these reference genomes.

They can identify the gene’s function, and identify which genus of bacteria the microbe belongs to. And by tallying all the genes they find, the scientists can estimate how abundant each type of bacteria is.

In the recent work, Dr. Bork and his team carried out an analysis of the gut microbes in 22 people from Denmark, France, Italy and Spain. Some of their subjects were healthy, while others were obese or suffered from intestinal disorders like Crohn’s disease. Dr. Bork and his colleagues searched for fragments of DNA corresponding to the genomes of 1,511 different species of bacteria. The researchers combined their results with previous studies of 13 Japanese individuals and 4 Americans.

The scientists then searched for patterns. “We didn’t have any hypothesis,” Dr. Bork said. “Anything that came out would be new.”

Still, Dr. Bork was startled by the result of the study: all the microbiomes fell neatly into three distinct groups.

And, as Dr. Bork and his colleagues reported on Wednesday in the journal Nature, each of the three enterotypes was composed of a different balance of species. People with type 1, for example, had high levels of bacteria called Bacteroides. In type 2, on the other hand, Bacteroides were relatively rare, while the genus Prevotella was unusually common.

“You can cut the data in lots of different ways, and you still get these three clusters,” Dr. Bork said.

Dr. Bork and his colleagues found confirmation of the three enterotypes when they turned to other microbiome surveys, and the groups continue to hold up now that they have expanded their own study to 400 people.

Correction Appended
In the early 1900s, scientists discovered that each person belonged to one of four blood types. Now they have discovered a new way to classify humanity: by bacteria. Each human being is host to thousands of different species of microbes. Yet a group of scientists now report just three distinct ecosystems in the guts of people they have studied.

Blood type, meet bug type.

“It’s an important advance,” said Rob Knight, a biologist at the University of Colorado, who was not involved in the research. “It’s the first indication that human gut ecosystems may fall into distinct types.”

The researchers, led by Peer Bork of the European Molecular Biology Laboratory in Heidelberg, Germany, found no link between what they called enterotypes and the ethnic background of the European, American and Japanese subjects they studied.

Nor could they find a connection to sex, weight, health or age. They are now exploring other explanations. One possibility is that the guts, or intestines, of infants are randomly colonized by different pioneering species of microbes.

The microbes alter the gut so that only certain species can follow them.

Whatever the cause of the different enterotypes, they may end up having discrete effects on people’s health. Gut microbes aid in food digestion and synthesize vitamins, using enzymes our own cells cannot make.

Dr. Bork and his colleagues have found that each of the types makes a unique balance of these enzymes. Enterotype 1 produces more enzymes for making vitamin B7 (also known as biotin), for example, and Enterotype 2 more enzymes for vitamin B1 (thiamine).

The discovery of the blood types A, B, AB and O had a major effect on how doctors practice medicine. They could limit the chances that a patient’s body would reject a blood transfusion by making sure the donated blood was of a matching type. The discovery of enterotypes could someday lead to medical applications of its own, but they would be far down the road.

“Some things are pretty obvious already,” Dr. Bork said. Doctors might be able to tailor diets or drug prescriptions to suit people’s enterotypes, for example.

Or, he speculated, doctors might be able to use enterotypes to find alternatives to antibiotics, which are becoming increasingly ineffective. Instead of trying to wipe out disease-causing bacteria that have disrupted the ecological balance of the gut, they could try to provide reinforcements for the good bacteria. “You’d try to restore the type you had before,” he said.

Dr. Bork notes that more testing is necessary. Researchers will need to search for enterotypes in people from African, Chinese and other ethnic origins. He also notes that so far, all the subjects come from industrial nations, and thus eat similar foods. “This is a shortcoming,” he said. “We don’t have remote villages.”

The discovery of enterotypes follows on years of work mapping the diversity of microbes in the human body — the human microbiome, as it is known. The difficulty of the task has been staggering. Each person shelters about 100 trillion microbes.

(For comparison, the human body is made up of only around 10 trillion cells.) But scientists cannot rear a vast majority of these bacteria in their labs to identify them and learn their characteristics.

As genetics developed, scientists learned how to study the microbiome by analyzing its DNA. Scientists extracted DNA fragments from people’s skin, saliva and stool. They learned how to recognize and discard human DNA, so that they were left with genes from the microbiome. They searched through the remaining DNA for all the variants of a specific gene and compared them with known species. In some cases, the variants proved to be from familiar bacteria, like E. coli. In other cases, the gene belonged to a species new to science.

These studies offered glimpses of a diversity akin to a rain forest’s. Different regions of the body were home to different combinations of species. From one person to another, scientists found more tremendous variety. Many of the species that lived in one person’s mouth, for example, were missing from another’s.

Scientists wondered if deeper studies would reveal a unity to human microbiomes. Over the past few years, researchers have identified the genomes — the complete catalog of genes — of hundreds of microbe species that live in humans. Now they can compare any gene they find with these reference genomes.

They can identify the gene’s function, and identify which genus of bacteria the microbe belongs to. And by tallying all the genes they find, the scientists can estimate how abundant each type of bacteria is.

In the recent work, Dr. Bork and his team carried out an analysis of the gut microbes in 22 people from Denmark, France, Italy and Spain. Some of their subjects were healthy, while others were obese or suffered from intestinal disorders like Crohn’s disease. Dr. Bork and his colleagues searched for fragments of DNA corresponding to the genomes of 1,511 different species of bacteria. The researchers combined their results with previous studies of 13 Japanese individuals and 4 Americans.

The scientists then searched for patterns. “We didn’t have any hypothesis,” Dr. Bork said. “Anything that came out would be new.”

Still, Dr. Bork was startled by the result of the study: all the microbiomes fell neatly into three distinct groups.

And, as Dr. Bork and his colleagues reported on Wednesday in the journal Nature, each of the three enterotypes was composed of a different balance of species. People with type 1, for example, had high levels of bacteria called Bacteroides. In type 2, on the other hand, Bacteroides were relatively rare, while the genus Prevotella was unusually common.

“You can cut the data in lots of different ways, and you still get these three clusters,” Dr. Bork said.

Dr. Bork and his colleagues found confirmation of the three enterotypes when they turned to other microbiome surveys, and the groups continue to hold up now that they have expanded their own study to 400 people.

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Consumption of polyunsaturated fatty acids, fish, and nuts and risk of inflammatory disease mortality

Background: n–3 (omega-3) Polyunsaturated fatty acids (PUFAs), fish, and nuts can regulate inflammatory processes and responses.

Objective: We investigated whether dietary intakes of PUFAs [n−3, n–6 (omega-6), and α-linolenic acid], fish, and nuts were associated with 15-y mortality attributed to noncardiovascular, noncancer inflammatory diseases.

Design: The analyses involved 2514 participants aged ≥49 y at baseline. Dietary data were collected by using a semiquantitative food-frequency questionnaire, and PUFA, fish, and nut intakes were calculated. Inflammatory disease mortality was confirmed from the Australian National Death Index.

Results: Over 15 y, 214 subjects died of inflammatory diseases. Women in the highest tertiles of total n−3 PUFA intake, compared with those in the lowest tertile of intake at baseline, had a 44% reduced risk of inflammatory disease mortality (P for trend = 0.03). This association was not observed in men. In both men and women, each 1-SD increase in energy-adjusted intake of α-linolenic acid was inversely associated with inflammatory mortality (hazard ratio: 0.83; 95% CI: 0.71, 0.98). Subjects in the second and third tertiles of nut consumption had a 51% and 32% reduced risk of inflammatory disease mortality, respectively, compared with those in the first tertile (reference). Dietary intakes of long-chain n−3 and n−6 PUFAs and fish were not associated with inflammatory disease mortality.

Conclusions: We report on a novel link between dietary intake of total n−3 PUFA and risk of inflammatory disease mortality in older women. Furthermore, our data indicate a protective role of nuts, but not fish, against inflammatory disease mortality.

Background: n–3 (omega-3) Polyunsaturated fatty acids (PUFAs), fish, and nuts can regulate inflammatory processes and responses.

Objective: We investigated whether dietary intakes of PUFAs [n−3, n–6 (omega-6), and α-linolenic acid], fish, and nuts were associated with 15-y mortality attributed to noncardiovascular, noncancer inflammatory diseases.

Design: The analyses involved 2514 participants aged ≥49 y at baseline. Dietary data were collected by using a semiquantitative food-frequency questionnaire, and PUFA, fish, and nut intakes were calculated. Inflammatory disease mortality was confirmed from the Australian National Death Index.

Results: Over 15 y, 214 subjects died of inflammatory diseases. Women in the highest tertiles of total n−3 PUFA intake, compared with those in the lowest tertile of intake at baseline, had a 44% reduced risk of inflammatory disease mortality (P for trend = 0.03). This association was not observed in men. In both men and women, each 1-SD increase in energy-adjusted intake of α-linolenic acid was inversely associated with inflammatory mortality (hazard ratio: 0.83; 95% CI: 0.71, 0.98). Subjects in the second and third tertiles of nut consumption had a 51% and 32% reduced risk of inflammatory disease mortality, respectively, compared with those in the first tertile (reference). Dietary intakes of long-chain n−3 and n−6 PUFAs and fish were not associated with inflammatory disease mortality.

Conclusions: We report on a novel link between dietary intake of total n−3 PUFA and risk of inflammatory disease mortality in older women. Furthermore, our data indicate a protective role of nuts, but not fish, against inflammatory disease mortality.

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