A healthy diet reduces the risk of type 2 diabetes, regardless of genetic predisposition.

A recent study by the University of Eastern Finland indicates that following a healthy diet based on nutrition recommendations is linked to improved blood glucose levels and a reduced risk of prediabetes and type 2 diabetes. This positive association was observed even among individuals with a high genetic predisposition to type 2 diabetes.

Type 2 diabetes is a strongly genetic disease that can be prevented and delayed with a healthy lifestyle, such as diet and exercise.

“However, we haven’t known whether a healthy diet is equally beneficial to all, i.e., to those with a low genetic risk and to those with a high genetic risk,” Doctoral Researcher Ulla Tolonen of the University of Eastern Finland says.

The cross-sectional study examined food consumption and blood glucose levels in more than 1,500 middle-aged and older men participating in the broader Metabolic Syndrome in Men Study, METSIM. Food consumption was measured using a food frequency questionnaire, and blood glucose levels were measured using a two-hour glucose tolerance test. In addition, study participants’ genetic risk of type 2 diabetes was scored based on 76 genetic variants associated with type 2 diabetes risk.

The researchers identified two dietary patterns based on food consumption. A dietary pattern termed “healthy” included, among other things, vegetables, berries, fruits, vegetable oils, fish, poultry, potatoes, unsweetened and low-fat yoghurt, low-fat cheese, and whole grain products, such as porridge, pasta, and rice. This diet was associated with, e.g., lower blood glucose levels and a lower risk of prediabetes and type 2 diabetes.

The study also explored the effect of the genetic risk of type 2 diabetes on the associations with diet and glucose metabolism. The associations of a healthy diet with better glucose metabolism seemed to hold for individuals with both a low and a high genetic risk of diabetes.

“Our findings suggest that a healthy diet benefits everyone, regardless of their genetic risk,” Tolonen concludes.

Study shows a high-fat diet may fuel anxiety

Junk Food
Junk Food

When stressed, many people turn to junk food for solace. However, new research by the University of Colorado Boulder suggests this strategy may backfire. 

The study found that in animals, a high-fat diet disrupts resident gut bacteria, alters behaviour and, through a complex pathway connecting the gut to the brain, influences brain chemicals in ways that fuel anxiety.

“Everyone knows that these are not healthy foods, but we tend to think about them strictly in terms of a little weight gain,” said lead author Christopher Lowry, a professor of integrative physiology at CU Boulder. “If you understand that they also impact your brain in a way that can promote anxiety, that makes the stakes even higher.”

Lowry’s team divided adolescent rats into two groups: Half got a standard diet of about 11% fat for nine weeks; the others got a high-fat diet of 45%, mostly saturated fat from animal products. 

According to the Centres for Disease Control and Prevention, the typical American diet is about 36% fat.

The researchers collected faecal samples throughout the study and assessed the animals’ microbiome or gut bacteria. After nine weeks, the animals underwent behavioural tests.

Not surprisingly, the high-fat diet group gained weight compared to the control group. However, the animals also showed significantly less diversity of gut bacteria. Generally speaking, more bacterial diversity is associated with better health, Lowry explained. They also hosted far more of a category of bacteria called Firmicutes and less of a category called Bacteroidetes. A higher Firmicutes to Bacteroidetes ratio has been associated with the typical industrialized diet and obesity.

The high-fat diet group also showed higher expression of three genes (tph2, htr1a, and slc6a4) involved in the production and signalling of the neurotransmitter serotonin—particularly in a region of the brainstem known as the dorsal raphe nucleus cDRD, which is associated with stress and anxiety.

While serotonin is often billed as a “feel-good brain chemical,” Lowry notes that certain subsets of serotonin neurons can, when activated, prompt anxiety-like responses in animals.  Notably, heightened expression of tph2, or tryptophan hydroxylase, in the cDRD has been associated with mood disorders and suicide risk in humans.

“To think that just a high-fat diet could alter the expression of these genes in the brain is extraordinary,” said Lowry. “The high-fat group essentially had the molecular signature of a high anxiety state in their brain.” 

Lowry suspects an unhealthy microbiome compromises the gut lining, enabling bacteria to slip into the body’s circulation and communicate via the vagus nerve, a pathway from the gastrointestinal tract to the brain.

“If you think about human evolution, it makes sense,” Lowry said.  “We are hard-wired to really notice things that make us sick so we can avoid those things in the future.” 

Lowry stresses that not all fats are bad and that healthy fats, such as those found in fish, olive oil, nuts, and seeds, can be anti-inflammatory and good for the brain.

His advice: Eat as many different kinds of fruits and vegetables as possible, add fermented foods to your diet to support a healthy microbiome and lay off the pizza and fries. Also, if you do have a hamburger, add a slice of avocado. Some research shows that good fat can counteract some of the bad.

The impact of lifestyle and diet on Rheumatoid Arthritis

Holistic approach to care
Holistic approach to care

The 16-week Plants for Joints trial investigated the effects of a multidisciplinary lifestyle intervention in people with RA compared to usual care. The intervention was based on a whole-food, plant-based diet alongside physical activity and stress management. Previous reports showed this intervention significantly reduced the 28-joint disease activity score (DAS28) compared to usual care alone.2,3 To expand on this, the researchers wanted to determine the long-term effectiveness of the intervention, specifically about disease activity after 2 years.

After the initial 16-week randomised period, the control group also received the intervention, and participants were followed for 2 years with biannual visits and six adherence-promoting webinars annually. People with DAS28 <2.6 also received a protocol as a suggested approach to tapering their antirheumatic medication – under the supervision of their rheumatologist – and any treatment changes were recorded.

62% of the original trial completers also completed the 2-year follow-up. Those who discontinued most often indicated that this was because they were too busy, unreachable, or did not permit for the second year of the extension study.

The long-term results showed that improvement in DAS28 was maintained for 2 years after completing the intervention – and was significantly lower compared to baseline. Tender joint count and general health components of the DAS28 also improved significantly, although there was no significant difference in the erythrocyte sedimentation rate and swollen joint count compared to baseline. Results were similar in people who completed the 2-year extension study versus those who discontinued prematurely.

Of the 39 participants who completed their follow-up and used disease-modifying antirheumatic medication, 44% could decrease or stop, 26% had stable usage, and 31% had increased medication. Of those with stable or decreased medication compared to baseline, 65% had improved DAS28.

After the 2-year follow-up, HDL cholesterol increased, and C-reactive protein (CRP) remained significantly lower compared to baseline values—although there was no longer a significant difference in weight, waist circumference, LDL cholesterol, or HbA1c.

These findings indicate that intensive lifestyle modifications can be effective in the long term for people with RA.