Sunlight Deprivation in Northern Latitudes: Reconciling Modern UK Lifestyles with Paleolithic Vitamin D Needs

Overview

Modern biological anthropology forces a stark physiological reckoning when examining the contemporary British population through an evolutionary lens. Genetically, our Pleistocene ancestors—optimised under equatorial and sub-Saharan ultraviolet radiation regimes—haroured high-capacity skin-synthesis machinery designed for continuous, high-flux cholecalciferol generation. When hominid migrations traversed into high-latitude northern ecosystems, severe selective pressures necessitated rapid depigmentation to maximize photon absorption across low-angle solar windows. Today, however, the inhabitants of the United Kingdom find themselves trapped in an evolutionary mismatch: an ancient, sun-adapted genome operating within a post-industrial indoor paradigm, compounded by geographic positioning above the 50th parallel north.

Epidemiological data from PubMed-indexed repositories and nationwide health audits consistently demonstrate that between the months of October and March, the zenith angle of the sun in the UK is insufficient to stimulate cutaneous previtamin D3 synthesis via UVB radiation (290–315 nm wavelengths). Photons are excessively scattered by the atmosphere's increased mass at these oblique angles, effectively creating a persistent "Vitamin D Winter." Compounding this geographical constraint is the modern British lifestyle, characterized by prolonged indoor sequestration, synthetic clothing barriers, and urban architectural occlusion. Consequently, ancestral physiological demands—which evolved to process upwards of 10,000 to 20,000 IU of cholecalciferol daily through full-body environmental exposure—clash directly with a sedentary society whose baseline dietary intake hovers near a fraction of these ancestral loads.

At INNERSTANDIN, our analysis of systemic biomarker data reveals that this chronic deprivation extends far beyond classical bone-mineral homeostatic failure, precipitating wide-ranging epigenetic and immunological dysregulation. Vitamin D receptors (VDRs) are ubiquitously expressed across human tissues, including the myocardium, neuroglia, and activated lymphocytes. When circulating 25-hydroxyvitamin D [25(OH)D] drops below optimal thresholds, the transcriptional activation of hundreds of vitamin D-responsive genes is compromised, impairing innate antimicrobial peptide production and skewing systemic inflammatory cytokine profiles.

Reconciling this biochemical dissonance requires viewing vitamin D not merely as a transient micronutrient, but as a potent steroid prohormone fundamental to human genome stability. Modern public health frameworks in the UK frequently underestimate the deep evolutionary latency programmed into our biology, treating insufficiency as a minor seasonal inconvenience rather than an ancestral emergency. To bridge this profound gap between Paleolithic physiological requirements and contemporary northern existence, we must dissect the precise photobiological mechanisms, genetic bottlenecks, and metabolic pathways that dictate human survival in the British Isles.

The Biology — How It Works

The human evolutionary trajectory is fundamentally tethered to photoperiodic exposure. For the vast majority of hominin history, survival dictated an outdoor existence, ensuring a steady, cyclical influx of ultraviolet B (UVB) radiation. When archaic humans migrated out of equatorial Africa into higher northern latitudes, radical evolutionary adaptations were required to maintain vitamin D homeostasis. Melanin pigmentation was progressively selected downward to maximise the penetration of scarce photons into the cutaneous matrix, initiating the photochemical synthesis of cholecalciferol. Today, the modern UK population faces an evolutionary mismatch: genomes optimised for ancestral hunter-gatherer UVB fluxes are now housed within indoor, urban environments situated above the 50th parallel north.

At the molecular level, vitamin D synthesis is initiated when UVB photons with wavelengths between 290 and 315 nanometres penetrate the stratum basale and spinosum of the epidermis. This specific energetic threshold is required to photolyse 7-dehydrocholesterol (provitamin $\text{D}3$) into previtamin $\text{D}3$, which subsequently undergoes a heat-dependent isomerisation to form cholecalciferol. Crucially, as documented extensively in epidemiological literature published in The Lancet, the zenith angle of the sun in the United Kingdom between October and March prevents UVB photons from piercing the atmospheric ozone layer in sufficient quantities. During this prolonged period, the skin’s capacity to synthesise endogenous cholecalciferol drops to absolute zero, irrespective of outdoor exposure duration.

Once generated or ingested, inert cholecalciferol enters the systemic circulation and undergoes a two-step enzymatic bioactivation process. First, hepatic microsomal enzymes—specifically the cytochrome P450 oxidase CYP2R1—hydroxylates the molecule at the carbon-25 position, yielding 25-hydroxyvitamin D ($\text{25(OH)D}$), the primary circulating biomarker quantified in clinical assays. Subsequently, a secondary hydroxylation occurs primarily within the proximal tubules of the kidneys, mediated by CYP27B1, to produce the biologically active steroid hormone 1,25-dihydroxyvitamin D ($\text{1,25(OH)}_2\text{D}$), or calcitriol.

Calcitriol exerts its genomic effects by binding to the nuclear Vitamin D Receptor (VDR). Upon heterodimerisation with the Retinoid X Receptor (RXR), this complex binds to specific Vitamin D Response Elements (VDREs) located within the promoter regions of target genes. Transcriptomic analyses reveal that over three percent of the human genome is directly or indirectly regulated by this signalling cascade. VDR expression is ubiquitous across human tissues, underscoring that vitamin D is not merely a regulator of calcium and phosphate homeostasis for skeletal integrity, but a systemic immune-modulator, epigenetic modifier, and cellular proliferation controller.

In the context of the UK’s geographic constraints, prolonged sunlight deprivation precipitates a chronic attenuation of VDR activation. Without adequate $\text{25(OH)D}$ substrates, autocrine and paracrine synthesis of calcitriol fails across non-renal tissues, including activated macrophages, osteoblasts, and epithelial barriers. This systemic failure disrupts innate immune responses—diminishing the up-regulation of antimicrobial peptides such as cathelicidin—and dysregulates inflammatory pathways by failing to suppress nuclear factor kappa B (NF-$\kappa$B) transcription. At INNERSTANDIN, our synthesis of the current biochemical literature highlights that chronic northern latitude deprivation is not simply a deficiency of a single micronutrient, but a profound systemic disruption of an evolutionarily conserved neuro-endocrine-immune network. Modern lifestyles have effectively severed the regulatory feedback loop between solar geometry and human transcription, necessitating a rigorous re-evaluation of how contemporary populations manage ancestral physiological requirements within artificial habitats.

Mechanisms at the Cellular Level

At the cellular and molecular tiers, the physiological friction between modern British lifestyles and our Paleolithic genetic blueprint is starkly evident. Homo sapiens evolved under equatorial and subtropical photon fluxes, developing a robust genomic apparatus dependent on solar ultraviolet-B (UVB) radiation. When this evolutionary anchor is severed—particularly across the 50°N to 60°N latitudes encompassing the United Kingdom—the downstream consequences cascade through nearly every human cell. The primary mediator of this cellular disruption is the secosteroid hormone cholecalciferol (Vitamin D3) and its transcriptionally active derivative, 1,25-dihydroxyvitamin D3 ($1,25(OH)_2D$).

Upon cutaneous synthesis or systemic supplementation, $1,25(OH)_2D$ binds to the intracellular Vitamin D Receptor (VDR), a ligand-activated transcription factor belonging to the nuclear receptor superfamily. Once heterodimerised with the retinoid X receptor (RXR), this complex translocates to the nucleus, binding to specific Vitamin D Response Elements (VDREs) within the promoter regions of target genes. Genomic mapping reveals that VDR binding sites regulate over three percent of the human genome, directly influencing cellular proliferation, differentiation, apoptosis, and immunological defence.

In the absence of adequate UVB photon absorption—exacerbated in the UK by persistent cloud cover, atmospheric scattering, and indoor-centric lifestyles—VDR activation plummets. At the immunological level, this deficit compromises both innate and adaptive pathways. Monocytes and macrophages rely on intracrine and paracrine synthesis of $1,25(OH)_2D$ to upregulate the transcription of antimicrobial peptides such as cathelicidin and defensin beta 2, which are essential for neutralizing intracellular pathogens. Furthermore, northern latitude sunlight deprivation skews systemic cytokine profiles, promoting a pro-inflammatory microenvironment characterized by elevated nuclear factor kappa B (NF-$\kappa$B) signalling and subsequent upregulation of interleukins IL-6 and TNF-alpha.

Mitochondrial bioenergetics are similarly perturbed. Emerging data published in peer-reviewed literature, including investigations indexed in PubMed, demonstrate that $1,25(OH)_2D$ modulates oxidative phosphorylation and mitigates the generation of reactive oxygen species (ROS) within the electron transport chain. Deprivation impairs this protective mitochondrial buffering, accelerating cellular senescence, epigenetic drift, and telomere attrition. In musculoskeletal tissues, insufficient active VDR ligands downregulate calcium-binding proteins (such as calbindin-D9k) within enterocytes and osteoblasts, impairing transcellular calcium transport and destabilising the structural integrity of the extracellular matrix.

For the contemporary UK population, this biochemical mismatch represents a profound evolutionary bottleneck. Without deliberate clinical synchronisation with our ancestral biological requirements, chronic photoperiodic deprivation locks the cellular machinery into a perpetual state of genomic downregulation, underpinning the high prevalence of metabolic, immunological, and degenerative pathologies observed across Britain today.

Environmental Threats and Biological Disruptors

The contemporary British phenotype operates under profound evolutionary dissonance, residing at latitudes where ambient ultraviolet B (UVB) photon flux remains biologically inert for nearly half the annual cycle. From an ancestral perspective, modern UK populations are experiencing an unprecedented physiological bottleneck. Epidemiological data published in The Lancet and indexed across PubMed consistently demonstrate that at latitudes north of 52°N—encompassing the entirety of the United Kingdom—the zenith angle of the sun between October and March is too oblique for UVB photons (290–315 nm) to penetrate the stratospheric ozone layer in quantities sufficient for cutaneous previtamin D3 synthesis. During these dormancy months, the human integumentary system is rendered functionally obsolete regarding photobiological hormone production.

This evolutionary mismatch is further compounded by what INNERSTANDIN defines as multi-layered environmental masking. The urbanised UK populace exists primarily within indoor, climate-controlled microenvironments bounded by architectural glass, which acts as an absolute spectral barrier to UVB wavelengths while permitting visible light transmission. Consequently, the endogenous synthesis of cholecalciferol is suppressed not merely by geographic determinism, but by behavioral enclosure. When individuals do transit through the British winter landscape, heavy sartorial shielding—mandated by thermal regulation—restricts cutaneous exposure to negligible surface areas of the facial and manual epidermis.

Furthermore, the biological cascade is heavily disrupted by contemporary anthropogenic stressors. Atmospheric particulate pollution, specifically particulate matter (PM2.5 and PM10) prevalent in British metropolitan conurbations, scatters and absorbs incoming UVB radiation, degrading the localized photon fluence rate. At the cellular level, this chronic photon deprivation initiates systemic dysregulation. Vitamin D receptor (VDR) expression, which governs over three percent of the human genome and modulates extensive immunogenomic pathways, becomes chronically under-liganded. Without adequate serum 25-hydroxyvitamin D [25(OH)D] thresholds—historically calibrated during Paleolithic epochs through unbroken diurnal exposure—innate and adaptive immune surveillance falters. Macrophage and monocyte activation pathways, which rely on intracrine and paracrine conversion of circulating 25(OH)D to its active metabolite 1,25-dihydroxyvitamin D to upregulate cathelicidin and defensin expression, are severely blunted. This molecular deficit underpins the well-documented seasonal surges in viral morbidity across the UK.

Compounding this environmental deficit is the pervasive modern burden of endocrine-disrupting chemicals and metabolic endotoxaemia, which accelerate the catabolism of circulating vitamin D metabolites via upregulation of hepatic cytochrome P450 enzymes (specifically CYP24A1). This enzymatic shunting prematurely degrades available pools of cholecalciferol, neutralizing even the marginal dietary inputs characteristic of the Western diet. Oily fish and fortified foodstuffs—often touted as compensatory UK public health interventions—fail to replicate the pulsatile, high-volume systemic bolus historically achieved via uninhibited solar radiation across large dermal expanses. Thus, the British population remains locked in a state of perpetual biochemical austerity, where the systemic architecture of the human organism is starved of the precise environmental inputs that shaped its genomic stability over millennia.

The Cascade: From Exposure to Disease

To truly comprehend the physiological devastation wrought by chronic sunlight deprivation across northern latitudes, we must examine the multistep biochemical cascade that couples environmental photon scarcity to systemic multi-organ pathology. In the evolutionary context of our Paleolithic forebears, intermittent high-intensity Ultraviolet-B (UVB) exposure at wavelengths between 290 and 315 nanometres photolysed 7-dehydrocholesterol in the stratum basale and spinosum of the epidermis into previtamin D3, which subsequently underwent thermo-isomerisation to cholecalciferol. Today, for populations inhabiting the UK—where solar zenith angles for roughly six months of the year preclude adequate UVB penetration through the atmospheric ozone layer—this evolutionary engine is effectively starved. As detailed in landmark epidemiological assessments from the UK Biobank and the Scientific Advisory Committee on Nutrition (SACN), systemic cholecalciferol insufficiency has become an entrenched phenotypic baseline for a staggering proportion of the British populace.

Once cholecalciferol synthesis stalls, the disruption cascades through the endocrine system. The liver-bound hepatic enzyme cytochrome P450 family 2 subfamily R member 1 (CYP2R1) hydroxylates the parent compound into 25-hydroxyvitamin D3 [25(OH)D], the primary circulating clinical biomarker. When substrate availability plummets, the subsequent renal and extra-renal conversion by CYP27B1 into the potent secosteroid hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D] is severely compromised. At INNERSTANDIN, our analysis of recent metabolomic profiling highlights that 1,25(OH)2D acts as a master genomic regulator, modulating the transcription of over two hundred genes through binding to the vitamin D receptor (VDR) and forming a heterodimer with the retinoid X receptor (RXR). When this nuclear signalling axis is chronically under-stimulated due to high-latitude photon starvation, the downstream consequences are profoundly systemic.

Without adequate nuclear VDR occupancy, intestinal calcium and phosphorus absorption efficiency drops from typical baseline levels of 30-40% down to a depleted 10-15%. To maintain strict physiological serum calcium homeostasis, the parathyroid glands upregulate the synthesis and secretion of parathyroid hormone (PTH). This secondary hyperparathyroidism induces osteoclastic bone resorption, leaching calcium and phosphate from the skeletal matrix to prop up extracellular fluid concentrations, thereby accelerating bone mineral density loss, osteomalacia, and osteoporotic fracture risk across the aging UK demographic.

Yet, the pathophysiological footprint of sunlight deprivation extends far beyond classical skeletal mineralisation defects. The VDR and the activating enzyme CYP27B1 are expressed ubiquitously across non-classical target tissues, including the endothelium, myocardium, pancreatic beta cells, and immune cells of both the innate and adaptive branches. Peer-reviewed investigations published in The Lancet and indexed across PubMed demonstrate that high-latitude hypovitaminosis D directly impairs macrophage antimicrobial peptide synthesis (such as cathelicidin and defensins), dampening pathogen clearance and skewing cytokine profiles toward chronic, low-grade systemic inflammation characterised by elevated C-reactive protein and interleukin-6. Concurrently, vascular smooth muscle dysregulation, renin-angiotensin-aldosterone system (RAAS) disinhibition, and endothelial nitric oxide synthase (eNOS) uncoupling driven by chronic VDR starvation accelerate arterial stiffness, precipitating the elevated cardiovascular morbidity and metabolic syndrome burdens disproportionately recorded in northern European cohorts. Reconciling our ancient, high-UVB ancestral genome with the indoor, high-latitude reality of modern British existence requires an unyielding, mechanism-first appreciation of this systemic biochemical unraveling.

What the Mainstream Narrative Omits

To truly grasp the contemporary UK health crisis driven by sunlight deprivation, one must first deconstruct the reductionist paradigms perpetuated by mainstream public health institutions. Standard dermatological and endocrinological guidance overwhelmingly frames ultraviolet (UV) exposure through a singular, myopic prism: the cutaneous synthesis of cholecalciferol (Vitamin D3) and the associated mitigation of squamous and basal cell carcinomas. This orthodox narrative fundamentally omits a vast network of non-calcemic photobiological mechanisms that evolved over millions of years of hominid exposure to high-intensity equatorial sunlight. Modern UK guidelines, which frequently recommend strict sun avoidance and the blanket use of high-factor topical sunscreens, ignore the evolutionary mismatch between our Paleolithic genome and indoor-centric British lifestyles.

At INNERSTANDIN, we examine the empirical literature to reveal that solar radiation is a systemic signaling molecule, not merely a carcinogen or a calciferol-factory. Beyond the well-documented hepatic and renal hydroxylation of Vitamin D into its active hormonal form, 1,25-dihydroxyvitamin D3, direct solar UVA and UVB exposure triggers immediate, non-vitamin-D-dependent physiological cascades. Research published in journals such as The Lancet and Cell demonstrates that dermal chromophores absorb photons to release pre-formed nitric oxide (NO) derivatives—such as nitrite and nitrosothiols—into the systemic circulation. This photolysis of cutaneous nitrogen oxides induces immediate, sustained vasodilation and lowers blood pressure independently of vitamin D status. Mainstream advisories that advocate total UV shielding inadvertently compromise this crucial cardiovascular protective mechanism, a particularly egregious oversight in a UK population already burdened by high rates of ischemic heart disease.

Furthermore, narrow-band and broad-band photon interactions with the skin modulate the human microbiome and systemic immune competence through the local production of antimicrobial peptides (AMPs) like cathelicidin, while also influencing regulatory T-cell (Treg) proliferation. Melanin and urocanic acid act as sophisticated photo-transducers, translating electromagnetic frequency into endocrine and neuroendocrine outputs, including the upregulation of pro-opiomelanocortin (POMC) cleavage products. These molecules govern circadian entrainment via the suprachiasmatic nucleus, modulate autonomic tone, and profoundly influence inflammatory pathways through the downregulation of nuclear factor kappa B (NF-$\kappa$B).

Epidemiological data from the UK Biobank underscore the perilous consequences of ignoring these broad-spectrum photobiological dependencies. Populations residing above the 50th parallel north experience a complete "vitamin D winter" from October to March, where the zenith angle of the sun prevents UVB photons of the necessary 290–315 nm wavelength from penetrating the atmospheric ozone layer. Yet, the mainstream insistence on oral supplementation as an equivalent substitute for solar exposure fails to account for these non-calcemic, photodynamic pathways. Supplementation corrects a molecular deficiency of a seco-steroid hormone, but it cannot replicate the systemic photo-immunological, cardiovascular, and neuroendocrine signaling triggered by broad-spectrum photons striking the integumentary system. Reconciling our biology with northern latitudes requires an urgent paradigm shift—moving away from a culture of absolute photon phobia and toward an evidence-based appreciation of ancestral light environments.

The UK Context

At northern geographical extremes—specifically between 50°N and 60°N, which encompasses the entirety of the United Kingdom—the physics of solar geometry imposes a profound metabolic bottleneck on human physiology. Epidemiological data published in The Lancet and indexed across PubMed consistently highlight that from October through March, the zenith angle of the sun is insufficient to facilitate cutaneous previtamin D3 synthesis. During this extended window, atmospheric ozone, particulate matter, and the elongated path length of UVB photons through the stratosphere result in the complete scatter and absorption of the crucial 290–315 nm ultraviolet spectrum. Consequently, dermal synthesis of cholecalciferol ceases entirely across the British Isles for nearly half the annual cycle, rendering the indigenous population entirely dependent on hepatic reserves and dietary influx.

This environmental constraint creates a profound evolutionary discordance. Genetically, our Paleolithic ancestors adapted to high-ambient-light equatorial and subtropical environments, where year-round UVB exposure maintained circulating 25-hydroxyvitamin D [25(OH)D] concentrations well above 75 nmol/L. Modern urbanised UK lifestyles, however, exacerbate this geographical deficit through hyper-indoor confinement, heavy reliance on artificial climate-controlled environments, and protective clothing protocols. Data from the National Diet and Nutrition Survey (NDNS) reveal that a significant proportion of Britons slip into deficient states (<25 nmol/L) during the winter months.

At INNERSTANDIN, we must interrogate the systemic physiological fallout of this mismatch. Vitamin D functions not merely as a fat-soluble vitamin, but as a potent secosteroid hormone regulating over 1,000 human genes via the widespread distribution of the vitamin D receptor (VDR). Chronic deprivation in the UK populace compromises innate and adaptive immunity—upregulating susceptibility to seasonal viral pathogens—impairs musculoskeletal integrity by precipitating secondary hyperparathyroidism, and disrupts neurosteroidogenesis implicated in seasonal affective disorder (SAD). Reconciling this modern epidemiological reality requires acknowledging that current public health thresholds are often inadequate for maintaining optimal genomic stability, demanding a rigorous re-evaluation of how northern populations navigate their ancestral biological requirements in a post-industrial landscape.

Protective Measures and Recovery Protocols

Reconciling the evolutionary mismatch of the British phenotype with contemporary northern latitudes requires multi-layered, evidence-led recovery protocols that extend far beyond simplistic supplementation models. From an ancestral perspective, Palaeolithic hominins in high-latitude environments would have relied heavily on seasonal fat-soluble nutrient storage and marine-dense foraging to bridge multi-month ultraviolet (UV) troughs. However, modern UK lifestyles—characterised by indoor urban habitation, atmospheric particulate scattering, and pervasive glass filtration—preclude endogenous cholecalciferol synthesis between October and April, driving systemic physiological dysregulation. Mitigating this chronic sunlight deprivation demands an integrative bioenergetic strategy that restores both endocrine and paracrine vitamin D signaling pathways without disrupting mineral homeostasis.

At the physiological core of this recovery framework is strategic, high-bioavailability supplementation paired with crucial enzymatic co-factors. As detailed in population health analyses within The Lancet, standard UK reference nutrient intakes are frequently insufficient to elevate 25-hydroxyvitamin D [25(OH)D] concentrations above the optimal 75 nmol/L threshold required for maximal extra-skeletal gene expression. Clinical interventions must utilise cholecalciferol (Vitamin D3) rather than ergocalciferol (D2), given the former's superior binding affinity to vitamin D-binding protein (DBP) and greater hepatic conversion efficacy. Yet, aggressive D3 administration in isolation risks precipitating functional magnesium and vitamin K2 deficiencies. Magnesium acts as an essential enzymatic cofactor for the hepatic 25-hydroxylase and renal 1-alpha-hydroxylase enzymes; without adequate intracellular magnesium, high-dose D3 remains unbioavailable or accelerates arterial calcification by failing to carboxylate matrix Gla-protein—a process fundamentally regulated by menaquinone-7 (Vitamin K2).

Furthermore, INNERSTANDIN research emphasizes that modern UK recovery protocols must look beyond isolated biochemistry to address circadian entrainment and mitochondrial resilience. Sunlight deprivation is not merely a photonic deficit of UVB wavelengths; it is a disruption of the broad-spectrum solar continuum that regulates suprachiasmatic nucleus signaling, melatonin synthesis, and cytochrome c oxidase activity within the mitochondrial electron transport chain. Therefore, advanced mitigation in high-latitude environments incorporates low-emf red and near-infrared (NIR) photobiomodulation therapy to partially mimic the mitochondrial signaling cascades usually initiated by natural solar exposure. Concurrently, dietary integration of wild-caught oily fish, pasture-raised ova, and organ meats re-establishes the ancestral lipid matrix necessary for optimal cellular membrane fluidity and hormone receptor sensitivity. By systematically addressing these biochemical bottlenecks, modern UK populations can effectively override the evolutionary friction of the northern European climate, restoring systemic homeostasis and immune-metabolic resilience at a cellular level.

Summary: Key Takeaways

The epidemiological data across the British Isles confirm a profound evolutionary mismatch: our Paleolithic genomic architecture, optimised for equatorial and low-latitude ultraviolet B (UVB) exposure, is systematically repressed by contemporary indoor-centric UK lifestyles and geographical zenith angles below 3° between October and March. This seasonal UVB attenuation halts cutaneous cholecalciferol synthesis, dropping systemic 25-hydroxyvitamin D [25(OH)D] concentrations below the critical 50 nmol/L physiological threshold across significant demographics. As explored throughout this INNERSTANDIN analysis, this deficit transcends simple skeletal pathology, disrupting over a thousand vitamin D-responsive genes governing neurosteroidogenesis, immune surveillance, and genomic stability. Chronic sunlight deprivation downregulates endogenous cathelicidin production, impairs T-cell receptor activation, and dysregulates dopaminergic and serotonergic pathways in the prefrontal cortex. To bridge this evolutionary chasm, modern public health frameworks must pivot from archaic supplementation baselines to precision, evidence-led interventions, acknowledging that restoring ancestral endocrine status is paramount for mitigating the chronic inflammatory phenotypes endemic to northern latitudes.