Dr. Weeks’ Comment: Perhaps your psychiatrist or primary care doctor who prescribed SSRI drugs for your loved one or yourself neglected to tell you that a safer and more effective option would be an anti-inflammatory agent… the safest and most beneficial of which is made from organic whole seeds!
BMC Med. 2013 Sep 12;11:200. doi: 10.1186/1741-7015-11-200.
So depression is an inflammatory disease, but where does the inflammation come from?
Berk M, Williams LJ, Jacka FN, O’Neil A, Pasco JA, Moylan S, Allen NB, Stuart AL, Hayley AC, Byrne ML, Maes M.
IMPACT Strategic Research Centre, School of Medicine, Deakin University, Geelong, VIC, Australia. email@example.com.
We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is ‘what is the source of this chronic low-grade inflammation?’
This review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.
The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.
PMID: 24228900 [PubMed – in process] Free full text
“…These results highlight the significant inflammatory and metabolic burden of individuals with depression…”
Inflammation, obesity, and metabolic syndrome in depression: analysis of the 2009-2010 National Health and Nutrition Examination Survey (NHANES).
To describe the rates of elevated inflammation, obesity, and metabolic syndrome (MetS) within a large cohort of individuals withdepression and to examine the interrelationships of inflammation and MetS in depressed individuals.
Analyses were conducted on study participants from the 2009-2010 National Health and Nutrition Examination Survey (NHANES) with Patient Health Questionnaire (PHQ-9) depression scores â‰¥ 10 to (1) examine the relationship of inflammation (C-reactive protein; CRP) with demographic and clinical characteristics and (2) examine the prevalence of MetS criteria within CRP groups.
5,579 participants provided PHQ-9 data; of those, 606 had PHQ-9 scores â‰¥ 10 and were included in further analysis. Of the 606 depressed participants, 585 participants had valid CRP data; 275 participants (47.01%) had CRP levels â‰¥ 3.0 mg/L, while 170 (29.06%) had CRP levels â‰¥ 5.0 mg/L. Elevated inflammation was significantly correlated with body weight, waist circumference, body mass index, insulin, 2-hour glucose tolerance, and self-report general health (P values < .05). 112 subjects (41.18%) met American Heart Association/National Heart, Lung, and Blood Institute criteria for MetS. Those with elevated CRP were more likely to meet criteria for MetS (odds ratios of 2.81 for those with CRP levels â‰¥ 3.0 mg/L and 1.94 for those with CRP levels â‰¥ 5.0 mg/L).
Over 29% of depressed individuals had elevated levels of CRP, and 41% met criteria for MetS. Individuals with elevated inflammationare more likely to be obese and meet criteria for MetS. These results highlight the significant inflammatory and metabolic burden of individuals withdepression.