This is a commentary arguing that rate of change in solar insolation, solar radiation measured in Watts, is responsible for seasonal changes in bipolar symptoms. An overarching critique of the paper is the paucity of references. Multiple claims are made in the paper that do not feel substantiated with sufficient evidence. More thorough review and incorporation of the literature feels needed in this paper in order to create a more persuasive argument. More evidence is needed to justify further investigation of the effects of solar insulation on the changes in mood and energy level among patients with bipolar disorder.

Specific comments:

(1) Suggest revealing the “hidden variable” (i.e., solar insolation) in the title for greater transparency.

(2) The introduction begins with a summary of seasonal patterns of symptoms in bipolar disorder. This is certainly an appropriate starting point, but please clarify whether these patterns (i.e., hypomania/mania in the spring and summer and MDEs in the fall/winter) pertain to bipolar disorders, in general, or to the proportion of bipolar cases that are seasonal affective disorder/meet criteria for the DSM-5 course specifier “With Seasonal Pattern.” I advise making this distinction and discussing seasonal patterns in both SAD and non-SAD bipolar disorder. Please provide references for the specific statements made throughout this section to be clear about the source of evidence for each, rather than a generically citing two papers at the very end of this paragraph (citations 1, 2).

(3) I enjoyed the general description of solar insolation, geographic differences in it at comparable latitudes, and other (weather-related) variables that can affect it. However, I think the following sentence refers to photoperiod, not solar insolation: “One can track changes in solar insolation from day to day by noting the times when the sun rises and sets.” Dusk to dawn hours is photoperiod, which differs from measures of luminosity including solar insolation.

(4) Please provide specific references for the predominant symptoms and sleep behaviors of mania/hypomania vs. of MDE in bipolar patients, rather than two generic references at the end of this paragraph (citations 3, 4). It is not clear if these sleep outcomes are derived from self-report sleep diary, actigraphy, or electroencephalography. In addition, insomnia is repeated three times (“insomnia, awakening at night, difficulty falling asleep”). “Awakening at night” could be labeled as middle insomnia, while “difficulty falling asleep” could be labeled as early insomnia. Not clear how the initial writing of “insomnia” differs from either of these constructs.

(5) The same two references (3, 4) are provided for the paragraph summarizing circadian phase dysregulation in bipolar patients? It seems that a great deal of the content of this commentary is based on reviews, making the reader wonder whether these thoughts are original. Please justify. In addition, it is unclear which phase(s) of the disorder (i.e. mania or depression) are associated with phase shifting of the circadian rhythm in melatonin.

(6) The discussion of lymphocytes is very informative as to the role of clock genes on bipolar disorder. An issue with this paragraph, however, is that it seems as though the focus shifts at the end of the paragraph to be concerned primarily with applicability and utility of lithium treatment. While this is informative for treatment, this is the only mention of lithium in the paper, and as such feels out of place.

(7) The paragraph starting, “Taken together, the compelling evidence in support of circadian disturbances in BD may also feed into seasonal influences relating to the onset of symptoms of mania or depression” seems out of place. It would be better to consolidate into the very beginning of the introduction, focused on seasonal presentation in bipolar disorders. Again, the same two references appear at the very end (3, 4). This paragraph includes a very generalized comment of seasonality not being pertinent to major depressive disorder. Making the claim that there is no seasonality in symptom of expression in major depressive disorder without any reference seems particularly egregious given the literature stating the opposite.

(8) Not clear how the premise proposed here is different from Bauer et al.’s (2014) “Relationship between sunlight and the age of onset of bipolar disorder: an international multisite study.” “Their rationale was that individuals who live greater distances from the equator would experience much greater changes in levels of solar insolation from winter compared to summer months and this greater amplitude of seasonal changes in light would impact BD symptom expression.” This commentary reviews the results of that investigation, which were supportive, at least for age of onset and suicide risk.

(9) The commentary tries to make a case for its novelty after reviewing Bauer et al. (2014): “But a key question still remains: what aspect of seasonal changes in solar insolation is measured as light is detected by specialized intrinsically photoreceptive retinal ganglion cells (ipRGCs) that express melanopsin and project to neurons in the suprachiasmatic nucleus (SCN), the master clock of the body?” I do not understand this statement; I suspect that there are words missing here.

(10) The commentary reviews a study already conducted by this group that examined monthly solar insolation, measured as global horizontal irradiance (GHI), in 51 cities for a year. “Sites in the northern hemisphere tended to attain maximum positive rates of change in GHI in the spring (February-May) and maximum negative rates of change in GHI in the fall (September-November). In contrast, locations in the southern hemisphere tended to attain maximum positive rates of change in GHI in the fall (September-November) and maximum negative rates of change in GHI in the spring (March-May).” This pattern of results maps onto what would be expected for rate of change photoperiod. The authors should speculate about whether rate of change in solar insolation is more important than rate of change in photoperiod for seasonality of bipolar. To tease this out, should not photoperiod be controlled for in examining the effect of solar insolation?

(11) The clinical implications at the end call into question the importance of clinicians tracking their local changes in solar insolation. It is suggested that treatment for bipolar “could be personalized such that therapeutic strategies employed during the transition from winter to spring (positive rates of change in solar insolation) might differ from strategies employed during the transition from summer to fall.” The same could be said of simply being mindful of changes in season and/or photoperiod, which is much easier to assess than solar insolation.

(12) The concluding paragraph surmises that the cues of solar insolation impact the onset, progression, intensity, and annual timing of bipolar disorder. The authors went into great detail of how solar insolation can relate to age of onset as well as annual timing of bipolar disorder, they did not provide evidence that would properly relate to intensity of bipolar symptoms.