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Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.
In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL_1 vs 11.28 [2.74] ng/mL_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.
For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.
What’s the issue?
Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?
Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.
In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL_1 vs 11.28 [2.74] ng/mL_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.
For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.
What’s the issue?
Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?
Over the past few years there have been studies published that support a relationship between acne and nutritional factors. Most suggest that high-glycemic-load diets and milk/dairy consumption might promote the development or exacerbation of acne vulgaris. So, what’s the mechanism? Some investigators believe that a high-glycemic-index diet induces hyperinsulinemia, which in turn elicits endocrine responses such as increasing androgen synthesis, ultimately inducing acne through mediators such as androgens, insulinlike growth factor (IGF) 1, and IGF binding protein 3. Insulinlike growth factor 1 itself can induce keratinocyte proliferation, sebocyte proliferation, and sebum production. We know that acne can be related to some endocrine diseases, such as polycystic ovary syndrome, which is characterized by peripheral insulin resistance and hyperinsulinemia, as well as acne, hirsutism, and androgenic alopecia.
In a study published by Çerman et al (J Am Acad Dermatol. 2016;75:155-162), investigators aimed to support the relationship between acne and diet and proposed that adiponectin levels, an adipocyte-derived hormone with established anti-inflammatory, antioxidant, and antidiabetic effects, are inversely associated with glycemic intake. Adiponectin inhibits proinflammatory cytokines, downregulates adhesion molecule expression, suppresses toll-like receptors and their ligands, and increases insulin sensitivity. In this small study of 50 patients with acne matched to 36 healthy controls, mean (SD) serum adiponectin concentrations were significantly lower in the patients with acne vulgaris than in the healthy controls (9.93 [2.29] ng/mL_1 vs 11.28 [2.74] ng/mL_1; P=.015), though milk and dairy product consumption, serum glucose, insulin, IGF-1, IGF binding protein 3, and homeostasis model assessment of insulin resistance values of the acne vulgaris and control groups did not differ significantly. The authors argued that this finding supports low-glycemic-load diets given the inverse correlation with adiponectin concentrations.
For every promising study comes one that may refute it. A study published online in February 2016 in Human & Experimental Toxicology aimed to evaluate several adipokines (adipocyte-derived cytokines) such as leptin, adiponectin, ghrelin and adiponectin levels, and adiponectin and leptin rates that indicate insulin resistance in nonobese patients with severe acne vulgaris. Although this study was smaller (30 acne patients and 15 controls), investigators found no difference between the 2 groups for any of these adipokines. It is important to note that patients studied were nonobese, nondiabetic, and glycemic load was not taken into account, so it is possible that this correlation is more significant for patients with factors such as insulin resistance and obesity.
What’s the issue?
Regardless of these findings, we have enough evidence to support that eating poorly can worsen acne and have other effects on the body. Are we all in agreement with this conclusion? Eating poorly is bad for more than just acne. High glycemic load leads to a proinflammatory state. Think psoriasis here. Chronic inflammation is detrimental for every organ system. Therefore, in addition to focusing on the pathways and elucidating the biology, let’s also design curricula to train current and future dermatologists how to counsel patients on diet or at the very least create resources to enable us to guide our patients. I published a survey study (J Am Acad Dermatol. 2014;71:1028-1029) showing that dermatologists are not comfortable counseling patients, specifically psoriasis patients, on diet, smoking, and drinking alcohol. It is time to create these tools. Do you want these types of resources?
