What is SAD?

Seasonal Affective Disorder is a recognised pattern of depression that follows a seasonal cycle, starting in autumn and improving in spring. ‘Actual’ SAD is a legitimate subtype of major depressive disorder with a seasonal pattern. The defining feature is timing. Symptoms return at roughly the same time each year for at least two consecutive years.

In winter-pattern SAD, symptoms typically include low mood, reduced motivation, increased sleep, carbohydrate cravings, weight gain, social withdrawal and a heavy, slowed-down feeling. It is not just “feeling a bit flat because it’s dark”. For some people, it is significant enough to impair work, relationships and daily functioning.

Of course, in popular culture people throw the term SAD about more loosely. Lots of people might use the phrase if they have a little low mood or are feeling glum, rather than if they’re experiencing the clinical disorder.

Why does SAD, or low mood in winter, happen?

The strongest explanation centres on light. Shorter days reduce light exposure, especially in the morning. Light directly influences circadian rhythm, melatonin timing and serotonin signalling. When light drops, circadian alignment can drift, melatonin can remain elevated for longer and serotonin activity can fall. In higher latitudes like the UK, this effect is more pronounced.

But here is the more interesting question.

If winter affects everyone’s light exposure, why do some people barely notice it while others feel like someone has turned the dimmer switch down on their brain?

As someone interested in the subject matter, and with my own personal genetics report in hand from Stride, let’s take a look. We’ll explore circadian genes, vitamin D pathways and methylation efficiency to see whether some people (me) may be more sensitive to winter than others.

My body clock: PER3 gene and chronotype

When people search “PER3 gene” or “PER3 gene chronotype morningness eveningness”, they are usually trying to understand why they feel more like a night owl or a morning person.

My results show a chronotype profile linked to variants in the PER3 gene and CLOCK gene chronotype pathways, pushing me more towards the night owl end of the spectrum. Indeed, it’s really easy for me to exercise at night or work late, and while I can just about scrape myself out of bed at a reasonable time, the spring doesn’t enter my step until a few hours later.

In simple terms, my internal body clock naturally runs later.

That matters more in winter than in summer.

Morning light is the main signal that anchors circadian rhythm. If you carry an evening-leaning PER3 variant, you already drift later in terms of when you’re most alert. When winter reduces early light exposure, that drift can become more pronounced. Melatonin clears more slowly. Alertness comes later. Mornings feel… sluggish.

For someone with this biology, shorter winter days are not neutral. They amplify an existing tendency, resulting in a daily routine that feels more challenging. While this is not SAD per se, it can be miserable.

What does VDR stand for, and why it matters in winter

As I look through the Google search analytics at Stride, I was surprised that people ask “what does VDR stand for” and “VDR test”. (I certainly didn’t know to Google this before getting my Stride DNA test.)

VDR stands for Vitamin D Receptor.

My Stride DNA nutrition report shows a raised genetic need for vitamin D, involving pathways linked to VDR signalling and vitamin D metabolism. If vitamin D molecules are ‘ships’ and the VDR is the harbour, my vitamin D ships may dock less efficiently than in people with other VDR variants. The solution? More boats. In other words, I may need to pay closer attention to maintaining adequate vitamin D levels.

People often confuse a VDR gene variant with a “VDR blood test”. They are different. A vitamin D blood test measures circulating 25(OH)D levels. A VDR gene test looks at genetic variants that may influence how vitamin D signalling functions at the cellular level.

Vitamin D and winter blues

In the UK, vitamin D production from sunlight effectively stops in winter. Vitamin D synthesis begins when UVB radiation from sunlight hits the skin and triggers a chemical reaction. In winter, because of the sun’s low angle, very little UVB reaches the UK’s surface. Bad news for vitamin D production.

If your genetics suggest you require more vitamin D for optimal function, that seasonal drop may have a greater impact.

Vitamin D receptors are present in brain tissue. Low vitamin D status has been associated with low mood and fatigue. So when light disappears in winter, two things happen simultaneously:

• The circadian system receives less anchoring light

• Vitamin D synthesis drops

For someone with a raised genetic need in the VDR pathway, that combination can feel heavier.

Methylation, MTHFR testing and my folate pathway

You might have heard of “MTHFR gene test”, “MTHFR mutation test” or “MTHFR testing”. But what do these have to do with a mood drop in winter or low-level SAD?

The MTHFR gene is part of the one-carbon metabolism pathway, which supports folate recycling and neurotransmitter synthesis.

In my case, the bigger signals are:

• MTHFD1 TT genotype

• MTR AA genotype

These variants are associated with reduced efficiency in the folate cycle. Folate metabolism feeds into the production of serotonin and dopamine. It also helps regulate homocysteine levels, which are associated with mood and cognitive health when elevated.

Winter lowers serotonin signalling for everyone. If the folate pathway that supports neurotransmitter production runs less efficiently, there may be less capacity to compensate for that seasonal drop.

Giving my biology the best chance

Individually, none of these gene variants are extreme. But stacked together:

• PER3 and CLOCK gene chronotype bias toward eveningness

• Raised vitamin D need linked to VDR pathways

• Reduced folate efficiency via MTHFD1 TT and MTR AA

Shorter winter days reduce circadian light input, decrease vitamin D synthesis and increase demand on neurotransmitter pathways at the same time. For someone with my profile, winter may simply be biologically more demanding.

So, what’s my strategy?

Like most health tests, whether Stride or a GP appointment, I use the results as fuel. I see them as areas where I need to double down to feel at my best.

Hence, in winter I prioritise:

• Early morning light exposure

• Proactive winter vitamin D supplementation

• Ensuring adequate folate intake (including methylated forms where appropriate)

• Sleep regularity (further supported by my Eight Sleep mattress)

What can you do?

You can do all of the above without genetic testing. But you might find it empowering to take a Stride DNA methylation test to understand whether you need to double down on morning sunlight or specific vitamin support to give yourself the best chance this winter — whether it’s a mild seasonal dip or fully developed Seasonal Affective Disorder.