I’m sure you’ll probably agree that one of the most common questions patients who have acne ask you is, “If I eat ____, will my acne get worse?”
I hear this question from patients, their parents, their grandparents or caregivers numerous times a week in my clinic. Mostly, they attribute acne to the cursed foods of French fries, chocolate, soda and pizza. Less often, milk or a variety of other foods get the blame.
The belief that certain foods or drinks are the culprits in causing acne is widely held, and when acne patients were surveyed, 32% felt that diet caused acne and 44% felt their diet aggravated acne.1
Design Flaws and Lack of Data in Studies
For the last 30 or more years, most dermatologists have told patients that acne is not caused by what they eat. These concepts came from two studies evaluating chocolate2 and chocolate bars, milk, peanuts and Coca-Cola3 and their role in causing acne.
The design flaws of these early studies have been extensively reviewed,4 but what such reviews do best is showcase the lack of data in the area. From the late 1960s/early 1970s up until a few years ago, there was little evaluation of the role diet plays on the development of acne. Recently, the idea has been revisited, mainly stemming from two studies, one implicating Western high glycemic load diets5 and the other implicating milk.6 (The controversy regarding milk and acne will be reserved for a future column.)
Cordain, et al., published observational data of two non-Westernized societies where no acne was seen in the subject populations, the Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay.5
They propose the lack of acne in the 1,315 subjects observed could not be attributed to genetics alone, but that a diet of tubers, fruit and fish and coconut by the Kitava, and of sweet manioc, peanuts, maize and rice with a smaller amount of Western pasta, flour, sugar, yerba tea and bread, led to no acne. It was postulated that these food items produced a low glycemic load, thus preventing a state of hyperinsulinemia.
Why Worry About Increased Insulin?
Well, insulin itself can stimulate a cascade of hormonal events including the increase of insulin-like growth factor 1 (IGF-1) and the decrease of insulin-like growth factor binding protein 3 (IGFBP-3).
How does this pertain to acne? We know that acne is a multi-factorial disease — cumulative follicular plugging from hyperproliferation of keratinocytes, increased sebum production, Propionibacterium acnes activity and inflammation.
IGF-1 may promote acne by inducing hyperkeratosis and epidermal hyperplasia as has been shown in mice,7 which is a step leading to the follicular plug. IGF-1 can also stimulate the production of androgens, well known to cause an increase in sebum. Clinically, direct injection of IGF-1 into women leads to acne.8
Finally, in post-adolescent women, aged 20 to 25 years, serum levels of IGF-1 were increased in those with acne,9 with further support of this recently presented showing that IGF-1 levels correlated positively with acne in older adult women (mean age 33 years).10
IGFBP-3 plays an inhibitory role in cell proliferation at the level of the follicle as it binds to the IGF receptor and doesn’t allow the IGF-1 to bind. Thus with increased levels of insulin, we have decreases in IGFBP-3, which then allow the IGF-1 to act.
Acne in Women Who Have Polycystic Ovarian Syndrome
So a link with IGF-1 and acne has been made, but the role of various hormones and the interactions between them is complex and remains to some extent, unknown. As mentioned above, the increased levels of IGF-1 are a part of a complex hormonal cascade involving androgens — both positively influencing the other. IGF-1 appears to stimulate androgens from gonadal tissues,11,12 and when early and late post menopausal women received treatment with dehydroepiandrosterone sulfate (DHEAS), they had increased levels of IGF-1.13
This leads to some of the best evidence we have for the role of diet and acne, in women with polycystic ovarian syndrome (PCOS). These patients often present with irregular menses, are often overweight, and infertile, and have masculine characteristics including alopecia and hirsutism. They can experience increased levels of insulin, be insulin resistant and hyperandrogenic. They also have increased levels of IGF-1.14
Increased levels of insulin in the patient with PCOS are known to be responsible for the high androgen concentrations. Androgens are known to play a major role in the pathogenesis of acne through stimulation of sebum production. The treatment for hyperinsulinemia can begin with weight loss, but pharmacological interventions are often needed. Oral hypoglycemic agents, such as metformin,15 tolbutamide,16 and pioglitazone,17 have been effective in improving insulin metabolism and reducing acne. A picture begins to emerge, but it must be remembered that the hormonal interactions are complicated and our knowledge is incomplete.
What Do We Tell Our Patients?
So what do we tell our patients in a concise way so that we educate them and dispel myths — while also remembering that most patients will hold on to their beliefs based on their own experiences?
• First, it’s essential to remind them that there’s a genetic component to acne.18 Regardless of all interventions, some patients will be more susceptible to the disease and to increased severity of the disease.
• We can tell them the jury is still out on the role of diet causing acne, and emphasize that the pathogenesis is multi-factorial. Therefore, no single treatment or habit change will rid them of the condition.
• We should not dismiss the patient who swears that certain foods cause acne and if a true dietary trigger is identified, avoidance should be practiced.
• Meanwhile, encourage all patients to eat the best diet to prevent well-documented disease states (cardiovascular disease, certain cancers), which are affected by diet. This will provide positive intervention.
• Remember the differences in medical conditions between the sexes. The adult woman, possibly overweight (but not necessarily so), who relates acne to her irregular menses, may benefit from an endocrinologic workup. This type of patient’s diet may be involved in her conditions. So, individualize your questions (for example, looking at age and sex), and with a few simple questions and observations we may be able to help the patient not only with her skin condition but with other medical problems.
• Finally, to tease out the complexities of what we eat and our physical being, we should encourage patients to participate in studies to elucidate the role of diet in the development of acne.
We have a way to go to understand how food affects our skin, but with well-controlled research we can add other solutions to our recipes for treatment.
I’m sure you’ll probably agree that one of the most common questions patients who have acne ask you is, “If I eat ____, will my acne get worse?”
I hear this question from patients, their parents, their grandparents or caregivers numerous times a week in my clinic. Mostly, they attribute acne to the cursed foods of French fries, chocolate, soda and pizza. Less often, milk or a variety of other foods get the blame.
The belief that certain foods or drinks are the culprits in causing acne is widely held, and when acne patients were surveyed, 32% felt that diet caused acne and 44% felt their diet aggravated acne.1
Design Flaws and Lack of Data in Studies
For the last 30 or more years, most dermatologists have told patients that acne is not caused by what they eat. These concepts came from two studies evaluating chocolate2 and chocolate bars, milk, peanuts and Coca-Cola3 and their role in causing acne.
The design flaws of these early studies have been extensively reviewed,4 but what such reviews do best is showcase the lack of data in the area. From the late 1960s/early 1970s up until a few years ago, there was little evaluation of the role diet plays on the development of acne. Recently, the idea has been revisited, mainly stemming from two studies, one implicating Western high glycemic load diets5 and the other implicating milk.6 (The controversy regarding milk and acne will be reserved for a future column.)
Cordain, et al., published observational data of two non-Westernized societies where no acne was seen in the subject populations, the Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay.5
They propose the lack of acne in the 1,315 subjects observed could not be attributed to genetics alone, but that a diet of tubers, fruit and fish and coconut by the Kitava, and of sweet manioc, peanuts, maize and rice with a smaller amount of Western pasta, flour, sugar, yerba tea and bread, led to no acne. It was postulated that these food items produced a low glycemic load, thus preventing a state of hyperinsulinemia.
Why Worry About Increased Insulin?
Well, insulin itself can stimulate a cascade of hormonal events including the increase of insulin-like growth factor 1 (IGF-1) and the decrease of insulin-like growth factor binding protein 3 (IGFBP-3).
How does this pertain to acne? We know that acne is a multi-factorial disease — cumulative follicular plugging from hyperproliferation of keratinocytes, increased sebum production, Propionibacterium acnes activity and inflammation.
IGF-1 may promote acne by inducing hyperkeratosis and epidermal hyperplasia as has been shown in mice,7 which is a step leading to the follicular plug. IGF-1 can also stimulate the production of androgens, well known to cause an increase in sebum. Clinically, direct injection of IGF-1 into women leads to acne.8
Finally, in post-adolescent women, aged 20 to 25 years, serum levels of IGF-1 were increased in those with acne,9 with further support of this recently presented showing that IGF-1 levels correlated positively with acne in older adult women (mean age 33 years).10
IGFBP-3 plays an inhibitory role in cell proliferation at the level of the follicle as it binds to the IGF receptor and doesn’t allow the IGF-1 to bind. Thus with increased levels of insulin, we have decreases in IGFBP-3, which then allow the IGF-1 to act.
Acne in Women Who Have Polycystic Ovarian Syndrome
So a link with IGF-1 and acne has been made, but the role of various hormones and the interactions between them is complex and remains to some extent, unknown. As mentioned above, the increased levels of IGF-1 are a part of a complex hormonal cascade involving androgens — both positively influencing the other. IGF-1 appears to stimulate androgens from gonadal tissues,11,12 and when early and late post menopausal women received treatment with dehydroepiandrosterone sulfate (DHEAS), they had increased levels of IGF-1.13
This leads to some of the best evidence we have for the role of diet and acne, in women with polycystic ovarian syndrome (PCOS). These patients often present with irregular menses, are often overweight, and infertile, and have masculine characteristics including alopecia and hirsutism. They can experience increased levels of insulin, be insulin resistant and hyperandrogenic. They also have increased levels of IGF-1.14
Increased levels of insulin in the patient with PCOS are known to be responsible for the high androgen concentrations. Androgens are known to play a major role in the pathogenesis of acne through stimulation of sebum production. The treatment for hyperinsulinemia can begin with weight loss, but pharmacological interventions are often needed. Oral hypoglycemic agents, such as metformin,15 tolbutamide,16 and pioglitazone,17 have been effective in improving insulin metabolism and reducing acne. A picture begins to emerge, but it must be remembered that the hormonal interactions are complicated and our knowledge is incomplete.
What Do We Tell Our Patients?
So what do we tell our patients in a concise way so that we educate them and dispel myths — while also remembering that most patients will hold on to their beliefs based on their own experiences?
• First, it’s essential to remind them that there’s a genetic component to acne.18 Regardless of all interventions, some patients will be more susceptible to the disease and to increased severity of the disease.
• We can tell them the jury is still out on the role of diet causing acne, and emphasize that the pathogenesis is multi-factorial. Therefore, no single treatment or habit change will rid them of the condition.
• We should not dismiss the patient who swears that certain foods cause acne and if a true dietary trigger is identified, avoidance should be practiced.
• Meanwhile, encourage all patients to eat the best diet to prevent well-documented disease states (cardiovascular disease, certain cancers), which are affected by diet. This will provide positive intervention.
• Remember the differences in medical conditions between the sexes. The adult woman, possibly overweight (but not necessarily so), who relates acne to her irregular menses, may benefit from an endocrinologic workup. This type of patient’s diet may be involved in her conditions. So, individualize your questions (for example, looking at age and sex), and with a few simple questions and observations we may be able to help the patient not only with her skin condition but with other medical problems.
• Finally, to tease out the complexities of what we eat and our physical being, we should encourage patients to participate in studies to elucidate the role of diet in the development of acne.
We have a way to go to understand how food affects our skin, but with well-controlled research we can add other solutions to our recipes for treatment.
I’m sure you’ll probably agree that one of the most common questions patients who have acne ask you is, “If I eat ____, will my acne get worse?”
I hear this question from patients, their parents, their grandparents or caregivers numerous times a week in my clinic. Mostly, they attribute acne to the cursed foods of French fries, chocolate, soda and pizza. Less often, milk or a variety of other foods get the blame.
The belief that certain foods or drinks are the culprits in causing acne is widely held, and when acne patients were surveyed, 32% felt that diet caused acne and 44% felt their diet aggravated acne.1
Design Flaws and Lack of Data in Studies
For the last 30 or more years, most dermatologists have told patients that acne is not caused by what they eat. These concepts came from two studies evaluating chocolate2 and chocolate bars, milk, peanuts and Coca-Cola3 and their role in causing acne.
The design flaws of these early studies have been extensively reviewed,4 but what such reviews do best is showcase the lack of data in the area. From the late 1960s/early 1970s up until a few years ago, there was little evaluation of the role diet plays on the development of acne. Recently, the idea has been revisited, mainly stemming from two studies, one implicating Western high glycemic load diets5 and the other implicating milk.6 (The controversy regarding milk and acne will be reserved for a future column.)
Cordain, et al., published observational data of two non-Westernized societies where no acne was seen in the subject populations, the Kitavan Islanders of Papua New Guinea and the Ache hunter-gatherers of Paraguay.5
They propose the lack of acne in the 1,315 subjects observed could not be attributed to genetics alone, but that a diet of tubers, fruit and fish and coconut by the Kitava, and of sweet manioc, peanuts, maize and rice with a smaller amount of Western pasta, flour, sugar, yerba tea and bread, led to no acne. It was postulated that these food items produced a low glycemic load, thus preventing a state of hyperinsulinemia.
Why Worry About Increased Insulin?
Well, insulin itself can stimulate a cascade of hormonal events including the increase of insulin-like growth factor 1 (IGF-1) and the decrease of insulin-like growth factor binding protein 3 (IGFBP-3).
How does this pertain to acne? We know that acne is a multi-factorial disease — cumulative follicular plugging from hyperproliferation of keratinocytes, increased sebum production, Propionibacterium acnes activity and inflammation.
IGF-1 may promote acne by inducing hyperkeratosis and epidermal hyperplasia as has been shown in mice,7 which is a step leading to the follicular plug. IGF-1 can also stimulate the production of androgens, well known to cause an increase in sebum. Clinically, direct injection of IGF-1 into women leads to acne.8
Finally, in post-adolescent women, aged 20 to 25 years, serum levels of IGF-1 were increased in those with acne,9 with further support of this recently presented showing that IGF-1 levels correlated positively with acne in older adult women (mean age 33 years).10
IGFBP-3 plays an inhibitory role in cell proliferation at the level of the follicle as it binds to the IGF receptor and doesn’t allow the IGF-1 to bind. Thus with increased levels of insulin, we have decreases in IGFBP-3, which then allow the IGF-1 to act.
Acne in Women Who Have Polycystic Ovarian Syndrome
So a link with IGF-1 and acne has been made, but the role of various hormones and the interactions between them is complex and remains to some extent, unknown. As mentioned above, the increased levels of IGF-1 are a part of a complex hormonal cascade involving androgens — both positively influencing the other. IGF-1 appears to stimulate androgens from gonadal tissues,11,12 and when early and late post menopausal women received treatment with dehydroepiandrosterone sulfate (DHEAS), they had increased levels of IGF-1.13
This leads to some of the best evidence we have for the role of diet and acne, in women with polycystic ovarian syndrome (PCOS). These patients often present with irregular menses, are often overweight, and infertile, and have masculine characteristics including alopecia and hirsutism. They can experience increased levels of insulin, be insulin resistant and hyperandrogenic. They also have increased levels of IGF-1.14
Increased levels of insulin in the patient with PCOS are known to be responsible for the high androgen concentrations. Androgens are known to play a major role in the pathogenesis of acne through stimulation of sebum production. The treatment for hyperinsulinemia can begin with weight loss, but pharmacological interventions are often needed. Oral hypoglycemic agents, such as metformin,15 tolbutamide,16 and pioglitazone,17 have been effective in improving insulin metabolism and reducing acne. A picture begins to emerge, but it must be remembered that the hormonal interactions are complicated and our knowledge is incomplete.
What Do We Tell Our Patients?
So what do we tell our patients in a concise way so that we educate them and dispel myths — while also remembering that most patients will hold on to their beliefs based on their own experiences?
• First, it’s essential to remind them that there’s a genetic component to acne.18 Regardless of all interventions, some patients will be more susceptible to the disease and to increased severity of the disease.
• We can tell them the jury is still out on the role of diet causing acne, and emphasize that the pathogenesis is multi-factorial. Therefore, no single treatment or habit change will rid them of the condition.
• We should not dismiss the patient who swears that certain foods cause acne and if a true dietary trigger is identified, avoidance should be practiced.
• Meanwhile, encourage all patients to eat the best diet to prevent well-documented disease states (cardiovascular disease, certain cancers), which are affected by diet. This will provide positive intervention.
• Remember the differences in medical conditions between the sexes. The adult woman, possibly overweight (but not necessarily so), who relates acne to her irregular menses, may benefit from an endocrinologic workup. This type of patient’s diet may be involved in her conditions. So, individualize your questions (for example, looking at age and sex), and with a few simple questions and observations we may be able to help the patient not only with her skin condition but with other medical problems.
• Finally, to tease out the complexities of what we eat and our physical being, we should encourage patients to participate in studies to elucidate the role of diet in the development of acne.
We have a way to go to understand how food affects our skin, but with well-controlled research we can add other solutions to our recipes for treatment.
