Kate McLintock general practitioner and visiting lecturer in primary care, Robbie Foy professor of primary care, Allan House professor of liaison psychiatry, Sarah L Alderson National Institute for Health Research clinical lecturer in primary care
McLintock K, Foy R, House A, Alderson S L.
A policy of universal screening for depression: caution needed
BMJ 2016; 353 :i2174
doi:10.1136/bmj.i2174
Screen for treatable biochemical abnormalities causing depression Re: A policy of universal screening for depression: caution needed
There is no need for caution in screening for the numerous and mostly treatable biochemical abnormalities which contribute to a high incidence of depression.1
A Search of PubMed brings up –
171 results for zinc deficiency and depression
141 results for magnesium deficiency and depression
100 results for vitamin B6 deficiency and depression
225 results for folic acid deficiency
229 results for vitamin B12 deficiency and depression
462 results for copper and depression
77 results for omega-3 deficiencies and depression
1133 results for progestins and mental depression
More recently there are 13 Search results for DNA hypomethylation and depression.
In 1968 we discovered that progestogen use is a major cause of depression in women. Both premenstrual progesterone or progestogenic hormonal contraceptives cause depressive mood changes which relate to increased monoamine oxidase (MA0) activity in the endometrium.2 In developed countries most women are given progestogenic hormonal contraceptives from young ages, usually without being monitored for essential nutrient deficiencies. Progestogens and oestrogens can cause B vitamin deficiencies, lower zinc and increase copper levels (but can lower copper stores) and increase adverse reactions to common food and chemicals, impair liver and pancreatic function, and, prevent absorption of essential nutrients before and pregnancy.3
Melas and Forsell found that depression in females is associated with hypomethylation in the first exon region of the monoamine oxidase A (MAOA) gene. They reported on a small-scale (n=44) replication study of MAOA methylation which confirmed that female subjects with a history of depression were hypomethylated compared to controls and showed that females were hypermethylated in the same region compared to males.4
Córdova-Palomera and colleagues found that in twins intrapair DNA methylation differences in an intron of DEPDC7 (chr11:33040743) were associated with intrapair differences in current depressive symptoms. Accordingly, a site-specific 10% DNA hypomethylation in a co-twin would correlate with a current depressive symptom score around 3.1 BSI (brief Symptom Inventory) points above the score of his/her less-depressed co-twin.5
There are numerous biomarkers which are important for understanding and treating depression and also many other conditions including vascular diseases and cancers.
1 McLintock K, Foy R, House A, Alderson SL. A policy of universal screening for depression: caution needed. BMJ 2016;353:i2174.
2 Grant EC, Pryse-Davies J. Effect of oral contraceptives on depressive mood changes and on endometrial monoamine oxidase and phosphatases. Br Med J 1968 Sep 28;3(5621):777-80.
3 Grant ECG. The pill, hormone replacement therapy, vascular and mood over-reactivity, and mineral imbalance. J Nutr Environ Med 1998;8(2):105-116.
4 Melas PA, Forsell Y. Hypomethylation of MAOA's first exon region in depression: a replication study. Psychiatry Res 2015 Mar 30;226(1):389-91.
5 Córdova-Palomera A, Fatjó-Vilas M, Palma-Gudiel H, Blasco-Fontecilla H, Kebir O, Fañanás L. Further evidence of DEPDC7 DNA hypomethylation in depression: A study in adult twins. Eur Psychiatry. 2015 Sep;30(6):715-8.
Competing interests: No competing interests