Stress may counteract the beneficial effects of a healthful diet, a study in Molecular Psychiatry suggests.
The study, a double-blinded randomized trial, looked at 58 women who first ate a meal high in saturated fats, the kind found in meat and butter. Then, one to two weeks later, the women ate a meal low in saturated fats. The only difference between the meals was in the ratio of saturated fats to unsaturated. In all other respects — number of calories, types of food, and amounts of fat, carbohydrate and protein — they were identical.
Before each meal, the women completed several well-validated questionnaires assessing symptoms of depression over the past week and the number of daily stressors in the past 24 hours. Researchers took blood samples before and after each meal.
Among women who had low levels of stress, markers of inflammation tended to be higher after eating the meal containing high levels of saturated fat than after the low saturated fat meal.
But for women who had high levels of stress, those differences disappeared — they had high levels of inflammation even after the meal that was low in saturated fats.
“The surprise here is that stress made the healthier-fat meal look like the saturated-fat meal,” said the lead author, Janice K. Kiecolt-Glaser, a professor of psychiatry at Ohio State University. “Stress is doing things with the metabolism that we really didn’t know about before.”
Depression, stress and diet can all alter inflammation. This double-blind, randomized crossover study addressed the impact of daily stressors and a history of major depressive disorder (MDD) on inflammatory responses to high-fat meals. During two separate 9.5 h admissions, 58 healthy women (38 breast cancer survivors and 20 demographically similar controls), mean age 53.1 years, received either a high saturated fat meal or a high oleic sunflower oil meal. The Daily Inventory of Stressful Events assessed prior day stressors and the Structured Clinical Interview for DSM-IV evaluated MDD. As expected, for a woman with no prior day stressors, C-reactive protein (CRP), serum amyloid A (SAA), intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) were higher following the saturated fat meal than the high oleic sunflower oil meal after controlling for pre-meal measures, age, trunk fat and physical activity.
But if a woman had prior day stressors, these meal-related differences disappeared—because the stressors heightened CRP, SAA, sICAM-1 and sVCAM-1 responses to the sunflower oil meal, making it look more like the responses to the saturated fat meal. In addition, women with an MDD history had higher post-meal blood pressure responses than those without a similar history. These data show how recent stressors and an MDD history can reverberate through metabolic alterations, promoting inflammatory and atherogenic responses.
Adherence to a Mediterranean-type diet can reduce the risk for depression, cardiovascular disease, type 2 diabetes and total mortality.1, 2, 3, 4 Reduced inflammation may be the cornerstone for the Mediterranean diet’s benefits.5, 6, 7, 8
The central fat source in the Mediterranean diet, olive oil, appears to be a key anti-inflammatory dietary component.8, 9 Indeed, a meta-analysis concluded that olive oil interventions lowered C-reactive protein (CRP) and interleukin 6 (IL-6) compared with control conditions.9 The major dietary fatty acids in the North American diet are palmitic acid, a saturated fatty acid found in meat and dairy products, and the monounsaturated oleic acid, the main fatty acid in olive oil, and many vegetable oils.10
Saturated fatty acids trigger proinflammatory signaling pathways.11 For example, palmitic acid activated toll-like receptor 4, leading to nuclear transcription factor-κB signaling and increased gene expression of IL-6, IL-8, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in contrast, the monounsaturated palmioleate did not have inflammatory sequelae.11 A meal made with butter, a rich source of saturated fatty acids, activated nuclear transcription factor-κB in peripheral blood mononuclear cells and also increased sICAM-1 concentrations, but a meal with olive oil, a rich source of oleic acid, did not.12 Palmitate-stimulated monocytes also fuel ICAM-1 expression in endothelial cells via an IL-1 signaling pathway.13
High saturated fat meals raise adhesion molecule concentrations while monounsaturated fat meals lower concentrations.
For example, high palmitate milkshakes boosted sICAM-1 levels while olive oil milkshakes decreased sICAM-1.14 Similarly, a high-palmitic fatty acid oil breakfast heightened post-meal sICAM-1 and sVCAM-1, but a refined olive oil breakfast lowered their concentrations. Postprandial sICAM-1 levels were amplified by a 12-week high saturated fat diet and reduced by a monounsaturated fat diet.
These meal-related differences are important because adhesion molecules play a central role in the development of atherosclerosis and diabetes.
Plasma sICAM-1 reflects a more generalized inflammatory process, while sVCAM-1 appears to be a better indicator of plaque burden.
In healthy people sICAM-1 serves as a more reliable prognostic indicator of cardiovascular disease than sVCAM-1, but sVCAM-1 better predicts cardiovascular events among patients with atherosclerotic disease than sICAM-1.17, 18, 19 Furthermore, adhesion molecules and inflammation are associated with an increased risk of hypertension and and monounsaturated fat interventions have reduced blood pressure.
Elevated sICAM-1 levels also predict type II diabetes.
For example, data from the Nurses’ Health Study showed that sICAM-1 independently predicted incident diabetes.21 In a large population-based prospective, sICAM-1 levels were higher among those participants who developed diabetes than in those who did not.20
In addition to these dietary fat influences, depression and stressors can also boost nuclear transcription factor-κB signaling, thus augmenting inflammation and increasing adhesion molecule concentrations.
For example, sICAM-1 levels were higher among all 18 physicians following an academic oral presentation compared with their own values 2 h earlier, as well as their data from parallel assessments obtained on a control day.
Comparisons of 22 patients who developed post-traumatic stress disorder following a myocardial infarction and 22 who did not develop post-myocardial infarction post-traumatic stress disorder showed that those with post-traumatic stress disorder had higher concentrations of sICAM-1 and sVCAM-1 at rest, as well as following a trauma-specific interview than their post-traumatic stress disorder-free counterparts.
Among patients who had experienced a recent acute coronary syndrome, sICAM-1 levels were higher among those with major depression than those who did not meet criteria.
Young adults with major depression had higher levels of sICAM-1 than nondepressed controls,34 and heightened sICAM-1 concentrations have also been found in healthy adults with elevated depressive symptoms.35, 36, 37, 38
People with a history of depression experience more major and minor stressors than those without a similar history, and past depression can also boost emotional reactivity to stressors.
Thus a mood disorder history could act synergistically with stress through multiple pathways.