- Consuming an unhealthy diet rich in sugars and fats can lead to obesity and also increase the risk of depression.
- A new study conducted in rats shows that exercise can help counter depressive and anxiety-like symptoms that result from a high-fat, high-sugar diet that is typical of a Western diet.
- However, exercise was not able to attenuate all the effects of the unhealthy diet, underscoring the importance of a healthy diet in addition to physical activity.
Exercise can help moderate some of the adverse effects of an unhealthy diet on depression-like symptoms in rats, according to a recent study published inBrain Medicine.
The study, conducted in a rat model, showed that exercise helped reduce depressive and anxiety-like symptoms induced by a high-fat, high-sugar diet.
The study’s findings suggest that exercise could mitigate the effects of an unhealthy diet on mood by normalizing levels of metabolic hormones, such as insulin and leptin, and attenuating the decline in certain metabolites produced by the gut microbiome.
The study’s lead author, Yvonne Nolan, professor in anatomy and neuroscience at University College Cork, said, “Our findings provide important proof-of-concept that exercise can mitigate some unhealthy diet-related mental health effects and point to specific biological pathways involved. More research is needed to confirm these effects in humans and understand the full mechanistic picture.”
The ease of access to ultra-processed foods that are high in sugar and saturated fats has led to an upsurge in obesity and other metabolic conditions. This increase in the prevalence of obesity has been compounded by the lack of physical activity and sedentary lifestyles.
Notably, the metabolic changes associated with the consumption of such a high-sugar, high-fat Western-style diet are also associated with an increased risk of mental health conditions, including depression and anxiety.
A high-fat, high-sugar Western-style diet can alter pathways involving metabolic hormones, including leptin and insulin, as well as the composition and metabolism of the gut microbiome.
Specifically, the consumption of ultraprocessed foods is associated with reduced gut microbiome diversity and the production of microbial metabolites that increase inflammation and alter brain function. These diet-induced changes in the gut microbiome and metabolic hormones have been shown to contribute to the effects of obesity on mental health.
In contrast, studies conducted in rodents have demonstrated that exercise can reduce depressive and anxiety-like symptoms while improving cognition. Exercise is associated with increased gut microbiome diversity and the production of microbial metabolites, such as short-chain fatty acids, which, in turn, are associated with a protective effect on mental health.
However, it is not known whether exercise can help attenuate or reduce the negative effects of a high-sugar, high-fat modern Western diet on mental health. The present study, conducted in young adult male rats, examined whether exercise could attenuate the effects of a high-sugar, high-fat cafeteria diet on mental health and metabolic changes.
“The research on the importance of diet and exercise on mental health is continuing to evolve. This study continues to add to the literature by showing the effects of voluntary exercise on a ‘cafeteria diet’ on depression, anxiety, and cognition.”
— Gia Merlo, MD, MBA, a clinical professor of psychiatry at the NYU Grossman School of Medicine, who was not involved in the study,
The animals in the study were either maintained on a standard diet or a cafeteria diet for 7.5 weeks. The cafeteria diet consisted of two high-fat and two high-sugar items, provided daily in addition to standard chow.
Half of the animals in the standard diet and cafeteria diet groups were assigned to the exercise group and had free access to a running wheel. The remaining half in each dietary group constituted the sedentary group.
The animals were subjected to an array of behavioral tests beginning at four weeks after the onset of the study. The researchers found that the cafeteria diet caused weight gain and increased fat mass in sedentary animals. Exercise resulted in a lower increase in weight and fat mass in rats maintained on the cafeteria diet.
The animals in the sedentary group fed a cafeteria diet showed increased depressive symptoms, and these effects were attenuated by exercise. Exercise also reduced anxiety-like behaviors and modestly improved spatial learning in both animals fed the standard diet and those maintained on the cafeteria diet.
At the end of the 7.5-week period, the researchers sacrificed the animals and obtained blood samples to measure the levels of metabolic hormones. The cafeteria diet increased insulin and leptin levels in sedentary animals. In contrast, exercise helped normalize insulin and leptin levels in animals maintained on the cafeteria diet.
The researchers used contents of the cecum, a part of the intestine rich in microbes, to assess changes in metabolites produced by the gut microbiota. They found that the cafeteria diet lowered the levels of three metabolites—anserine, indole-3-carboxylate, and deoxyinosine — in both the sedentary and exercise groups.
However, exercise helped reduce the decline in levels of these metabolites in the cafeteria diet group. Notably, these metabolites produced by the gut microbiota have been shown to modulate the nervous system.
Anserine has antioxidant and anti-inflammatory properties and has been shown to have the potential to reduce depressive symptoms and
The aforementioned changes in metabolic hormones and metabolites suggest these could be potential pathways through which exercise could mitigate the effects of an unhealthy diet.
The researchers also extracted the brains of the sacrificed animals to quantify the generation of new brain cells (neurons) in the hippocampus, a brain region involved in memory, learning, and mood regulation.
Studies have shown that the generation of new cells in the hippocampus is associated with improvements in depression and memory formation. Moreover, previous studies suggest that an unhealthy diet impairs the generation of new brain cells in the hippocampus, whereas exercise increases their proliferation in this brain region.
In the present study, the researchers found that exercise increased the number of newly generated neurons in the hippocampus of rats fed standard chow, but not in those fed a cafeteria diet. This result suggests that a combination of exercise and a healthy diet may be necessary to induce the generation of new nerve cells in the hippocampus.
“While exercise is the lifestyle intervention with the most data supporting improvement in depression and anxiety, this study implies that exercise alone may not be sufficient, but a healthy diet is also necessary,” Merlo said.
Similarly, cafeteria food increased the levels of metabolic hormone fibroblast growth factor-21 (FGF-21) in both the sedentary and exercise groups. In other words, exercise was not able to counteract the effects of an unhealthy diet on FGF-21.
Together, these results suggest that exercise cannot counteract all the negative effects of an unhealthy diet.
In an editorial published in the same issue of Brain Medicine, Julio Licinio, MD, PhD, and colleagues note that while exercise does not attenuate all the changes caused by an unhealthy diet, it could be a first step toward losing weight and improving mental health.
“Patients often start moving before they can change their diet. When they feel better, diet becomes more approachable. Increased sleep and less despair lead to a person making a better breakfast. By accepting that the effect size unambiguously depends on the biology, we can design achievable treatment sequences: start with what is doable (walking, stationary cycling, light resistance), stack modest dietary improvements, and let the physiology turn in your favour.”
— Julio Licinio and colleagues
However, the study’s results must be interpreted cautiously as human studies are still needed.
“We studied young adult male rats only. While animal models provide valuable mechanistic insights, we cannot assume identical effects in humans, females, or different age groups,” Nolan said.
Highlighting the challenges of translating results from animal studies to humans, Nolan noted, “Our rats exercised voluntarily with continuous wheel access, which differs from structured human exercise programs.