Is it time to reassess current safety standards for glyphosate-based herbicides? 


Use of glyphosate-based herbicides (GBHs) increased ∼100-fold from 1974 to 2014. Additional increases are expected due to widespread emergence of glyphosate-resistant weeds, increased application of GBHs, and preharvest uses of GBHs as desiccants. Current safety assessments rely heavily on studies conducted over 30 years ago. We have considered information on GBH use, exposures, mechanisms of action, toxicity and epidemiology. Human exposures to glyphosate are rising, and a number of in vitro and in vivo studies challenge the basis for the current safety assessment of glyphosate and GBHs. We conclude that current safety standards for GBHs are outdated and may fail to protect public health or the environment. To improve safety standards, the following are urgently needed: (1) human biomonitoring for glyphosate and its metabolites; (2) prioritisation of glyphosate and GBHs for hazard assessments, including toxicological studies that use state-of-the-art approaches; (3) epidemiological studies, especially of occupationally exposed agricultural workers, pregnant women and their children and (4) evaluations of GBHs in commercially used formulations, recognising that herbicide mixtures likely have effects that are not predicted by studying glyphosate alone.


Glyphosate is an active ingredient in a number of commercially available herbicides, including several that are used in concert with genetically modified crops. The herbicidal action of glyphosate derives from its inhibition of a key plant enzyme, 5-enolpyruvylshikimate-3-phosphate synthase, which is involved in the synthesis of aromatic amino acids. Since this enzyme is not present in vertebrates, it has long been believed that glyphosate would not affect non-target species, including humans. However, multiple lines of evidence suggest that this contention is inaccurate.

Methods used in environmental health sciences to examine the potential health effects of chemicals, including pesticides, have undergone substantial changes over the past 30 years. Cutting-edge tools currently employed by federally funded scientists bear little resemblance to the archaic standardised assays required by regulatory agencies and used in formal risk assessments.1 We are concerned that the assays used to assess glyphosate safety, including the toxicity studies requested by the US Environmental Protection Agency (EPA) in 2009, may be insufficient to address the full complement of health effects that could be induced by exposure to glyphosate-based herbicides (GBHs).

In this commentary, we summarise these key findings as well as trends in increased use of GBHs. Since commercial applications of GBHs began four decades ago, their use has diversified and expanded considerably. We offer recommendations on how to reduce significant uncertainties concerning GBH risks.

Glyphosate use has increased since safety evaluations were conducted

Glyphosate was registered in 1974 in the USA as a broad-spectrum contact herbicide to kill weeds in fields prior to the planting of crops. It was also approved for weed control in a variety of non-crop settings. Glyphosate use is the highest of any pesticide in the USA, with rapid increases in use over the last two decades; worldwide estimates of use suggest that enough GBH was applied in 2014 to spray nearly 0.5 kg glyphosate on every hectare of cropland on the planet.2

In addition to their use as weed-control herbicides, GBHs are now used as desiccants prior to harvest3 to accelerate natural drying of seeds. These use patterns are expected to increase glyphosate residue levels in harvested products. Although such effects still need to be evaluated in controlled studies, residues of glyphosate and aminomethylphosphonic acid (AMPA) (the major bioactive metabolite of glyphosate) are now routinely detected in soybeans, wheat, barley, and many other crops and foods.4 ,5

Although GBH use has increased dramatically in the last 10 years, most of the science used in the risk assessment process to support its safety was conducted more than 30 years ago. In the US EPA’s 1993 registration review of GBHs,6 for example, 73% of the almost 300 citations were published prior to 1985; importantly, only 11 were peer-reviewed. A search of PubMed (conducted 6 November 2016) reveals more than 1500 published studies on glyphosate in the last decade alone. It is incongruous that safety assessments of the most widely used herbicide on the planet rely largely on fewer than 300 unpublished, non-peer-reviewed studies while excluding the vast, modern literature on glyphosate effects.

Considering the ∼100-fold increase in GBH use in the last four decades, increased human exposure is almost certain. Unfortunately, no systematic data have tracked changes in glyphosate or AMPA concentrations in human tissues or bodily fluids during this period. For this reason, we recommend that glyphosate and AMPA should be monitored by the US Centers for Disease Control and Prevention (US CDC) in its National Health and Nutrition Examination Survey (NHANES) biomonitoring programme, as well as other biomonitoring programmes around the world. Studies of the general population to evaluate actual exposures via diet (rather than hypothetical inferred exposures), as well as studies in occupationally exposed individuals (eg, pesticide sprayers as well as production workers), are both needed.

Are humans affected by GBHs?

There are few human epidemiology studies examining the impact of glyphosate on human diseases. Unexplained chronic kidney disease has killed thousands of rice farm workers in Sri Lanka7 and sugarcane workers in Central America;8 exposure to herbicides including GBHs has been documented in some of these populations.9 Some epidemiologists have hypothesised that epidemics of chronic kidney disease among male agricultural workers result from the interactions of the herbicide with hard drinking water and associated metals.7 ,9 Others have attributed these health conditions to dehydration.10 Neither explanation is plausible because such plantation work in these regions has been going on for centuries while the epidemic of kidney failure and herbicide use are recent phenomena.

A number of other studies have evaluated the association between exposures to GBHs and other health effects in humans including cancer. In fact, some of the most compelling studies in human populations suggest associations between GBHs and non-Hodgkin lymphoma.11 ,12 Cancer end points will be discussed later in this commentary.

Without appropriate epidemiological and biomonitoring studies, any association between glyphosate and AMPA concentrations found in human tissues and fluids with disease will remain uncertain. Epidemiological studies are urgently needed to augment the ability of risk assessors to draw better conclusions about the safety of GBHs. Such studies should evaluate short-term and long-term health outcomes including DNA damage and cancer.

Recent studies raise new questions about GBH safety

In laboratory animals, glyphosate can disrupt reproductive development in male rats,13 and male and female fish.14 ,15 Studies in fish and the amphibian Xenopus laevis demonstrate that developmental exposures to GBHs induce malformations in craniofacial structures and the brain, although the mechanism underlying these effects is not fully understood.16 ,17 Research from controlled laboratory studies also suggests that GBHs may contribute to liver,18 hepatorenal19–22 and cardiovascular damage;23 ,24 some of these effects may be due to altered ion flux in these tissues.25 GBHs are also recognised to cause serious eye damage based on evaluation of six separate studies.26 Finally, GBH exposures have been shown to induce oxidative stress27 and genotoxicity28 in vitro and in vivo.

In a previous consensus statement, we analysed these data and raised concerns over the setting of ‘safe’ levels of exposure by regulatory agencies around the world;29 other comprehensive reviews of the toxicity literature also provide an excellent overview of the effects of glyphosate and GBHs on a range of end points.30 ,31

Recently, there has been debate over the possibility that glyphosate is an endocrine disruptor.13 ,14 ,32–34 Studies in cell culture showed that glyphosate induces endocrine-mediated effects on end points relevant to toxicity, as well as cell proliferation.32 ,33 In contrast, using their Endocrine Disruptor Screening Program (EDSP), the US EPA’s recent review of glyphosate dismissed statistically significant differences consistent with oestrogenic activity in some assays (eg, altered vitellogenin levels in a fish short-term reproduction assay) because they followed a non-monotonic dose response.35 The final conclusion of the US EPA was that ‘there was no convincing evidence’ that glyphosate interacts with endocrine pathways. Significant criticisms of the EDSP assays have been raised by endocrinologists, and others have expressed concern about the failure of the EPA to acknowledge non-monotonic dose responses, which have been documented for other endocrine disruptors.36 Other agencies including the European Food Safety Authority (EFSA) have used the EDSP data to suggest that there is not sufficient evidence to conclude that glyphosate is an endocrine disruptor, but the 2015 EFSA report does note that ‘signs of endocrine activity… could not be completely ruled out’ in some of these assays.37

In December 2009, the US EPA issued a ‘Glyphosate Final Work Plan (FWP) registration review’38 that identified uncertainties about the toxicity of glyphosate. For example, the EPA announced its plan to require that registrants conduct acute and subchronic neurotoxicity studies as well as an immunotoxicity study. The EPA also acknowledged that AMPA had not been evaluated for ecological risk assessments. Since this testing is supposed to be conducted by the registrants, it is unclear whether testing is underway, will actually be completed, or will be published in the peer-reviewed literature. Thus, additional studies, using state-of-the-art approaches, are needed to better elucidate the effects of glyphosate and GBHs on non-target species. We recommend that scientists and entities independent of the registrants, (eg, the US National Toxicology Program (NTP)) should prioritise glyphosate and GBHs for hazard assessments. In fact, the US EPA also proposed a collaborative research plan with the NTP, which calls for NTP to help provide answers to four research questions: (1) comparisons of the toxicity of glyphosate versus GBH formulations; (2) provide publicly available data on glyphosate’s effects on cancer-related end points; and (3) non-cancer end points; (4) finally, investigate the mechanisms by which glyphosate and GBHs induce toxic and adverse effects.39 Several of these points are addressed further below.

GBHs are chemical mixtures, and may be more toxic than glyphosate alone

GBHs are always used as a mixture of glyphosate plus numerous other so called inert ingredients, which are added to alter the herbicide’s physicochemical properties and enhance its herbicidal action. Some inert ingredients or chemicals are used to enhance the adhesion of glyphosate to plant surfaces (eg, alkyl polyglycosides), whereas others facilitate its penetration of plant cell walls and into plant tissues (eg, ethoxylated tallow amines) to exert its herbicidal effects. Unfortunately, the full list of these chemicals, collectively known as adjuvants or coformulants, is treated as a trade secret by the manufacturers; the composition of GBHs are unknown and available data on the hazards posed by different mixtures remain limited.

Chemical mixtures can have effects that are more potent than the effects of individual ingredients.40 GBHs have been shown to be more toxic than glyphosate.41–44 It also should be noted that some of the studies discussed in the previous section of this review evaluated GBHs, and thus likely reveal effects that may not be observed if studies examined only the active ingredient. These results reveal that GBH safety evaluations focused on glyphosate alone can underestimate toxicity and are insufficient to assess relevance to human and environmental exposures. Although the number of commercial formulations is extensive and will be difficult to study comprehensively, we propose that the most widely applied GBH formulations should be tested in parallel with glyphosate alone.

Is glyphosate a human carcinogen?

Over the last few years, glyphosate has received significant attention by the public as well as regulatory agencies around the world. In the European Union, safety evaluations on glyphosate have recently been conducted by the European Chemicals Agency (ECHA) and EFSA; in the USA, meetings by evaluation committees within the US EPA scheduled for fall 2016 were cancelled so the agency could supplement the panel of experts with additional members who have expertise in epidemiology. In December 2016, an EPA scientific advisory panel was charged with evaluating the human carcinogenic potential of glyphosate only, not GBHs. The conclusions of this panel have not yet been released.

The WHO’s International Agency for Research on Cancer (IARC) working group’s 2015 decision to classify glyphosate as a grade 2A probable human carcinogen followed an extensive review and evaluation of the weight of all available evidence.45 The outcome was driven by: (1) limited human evidence from case–control epidemiology studies, including high-quality studies reporting a link with non-Hodgkin lymphoma;11 ,12 (2) sufficient evidence from unpublished animal studies analysed by the US EPA, which identified an elevated frequency of rare kidney tumours in male mice, hemangiosarcoma in male mice, pancreatic islet-cell adenoma in male rats, and skin tumours and other non-malignant growths in mice and (3) strong mechanistic evidence, such as numerous studies demonstrating that glyphosate is genotoxic and can induce oxidative stress in humans, human cells, non-human mammals and non-mammalian species (data reviewed in depth in ref. 46). Other data from unpublished studies that have been reviewed in the peer-reviewed literature could not be evaluated by IARC because the data were not publicly available; some of these studies also suggest increases in lymphoma in male mice exposed even to the lowest doses evaluated (14.5 mg/kg/day) (see study 13 evaluated in ref. 47).

A joint meeting on pesticides residues (JMPR) in the WHO used the IARC hazard assessment evaluation (eg, concluding that glyphosate is a probable human carcinogen) to establish a safe level of exposure for humans. In their most recent evaluation, JMPR would not exclude the possibility that glyphosate is a human carcinogen, but concluded that it ‘is unlikely to pose a carcinogenic risk to humans from exposure through the diet’.48 The JMPR did not conduct a quantitative assessment to estimate cancer risk at current dietary exposures, and, more crucially, did not evaluate actual dietary exposures in any population.

The IARC classification was made based on an analysis of the entire body of evidence, including the evaluation of GBH (mixtures) and not glyphosate alone, as IARC requires that ‘the body of evidence is considered as a whole…’.49 A 2016 review of the carcinogenic potential of glyphosate by EFSA contrasts with the IARC conclusions.37 EFSA concluded that ‘glyphosate is unlikely to pose a carcinogenic hazard to humans’ but notes that it drew its conclusions based only on studies of glyphosate alone; studies of GBHs were not included in the EFSA assessment. Other agencies in the European Union, including the German Federal Institute for Risk Assessment, have similarly focused on studies of the active ingredient, failing to consider all studies of GBHs.50 Furthermore, the EFSA monograph notes that studies that demonstrate the genotoxicity of glyphosate that were considered by IARC were not considered by EFSA because they did not follow prescribed guidelines for study reporting (eg, good laboratory practices, or GLP);37this argument has also been made to eliminate studies conducted within academia in other risk assessments,1 despite evidence that academic laboratory research can be well designed and properly reported in the absence of GLP.51 Importantly, studies conducted according to GLP (including study 13 evaluated in ref. 47) that suggest causal links between glyphosate and cancer in exposed rodents have been dismissed by agencies including the EPA and EFSA due to speculation about a viral infection in the animal colony, even though no adverse health effects of such an infection have been shown.26

After the release of the IARC and EFSA expert conclusions, there were a number of public discussions and articles written for lay audiences describing how these organisations could come to conflicting results after reviewing the same literature. These discussions revealed that the same literature often was not evaluated: IARC examined studies of GBH and glyphosate whereas EFSA only evaluated studies of glyphosate; IARC examined all studies whereas EFSA gave priority to studies conducted according to GLP. Finally, IARC has strict conflict of interest rules about the experts that serve on its panels, whereas other agencies including EFSA do not exclude experts that have received monetary compensation from chemical manufacturers. There is evidence that the presence of individuals with conflicts of interest on regulatory panels can influence the integrity of decision making.52 ,53

Where does the burden of proof of safety lie?

The EFSA report, evaluating only studies of glyphosate and not GBH mixtures, concluded that there was no evidence to conclude that it is a carcinogen.37 The European Commission has not yet accepted the EFSA conclusion; in 2016, because European Union member states failed to take action against glyphosate, the European Commission extended its approval for its use under certain circumstances for 18 months, giving ECHA this time to review glyphosate’s classification. In the interim, the Commission recommended that an adjuvant, ethoxylated tallow amine, be banned from GBHs; that spraying of public parks, playgrounds and gardens be minimised; and that preharvest uses be minimised.54 It will be up to the individual member states to approve and enforce these recommendations.

In the USA, the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA, (7 U.S.C. §136 et seq. (1996))) requires chemical manufacturers to demonstrate that a pesticide will not cause ‘unreasonable adverse effects on the environment’. Although FIFRA allows risks to humans and the environment to be balanced by the benefits of a pesticide’s use, this can only be accomplished if sufficient data are available to support safety. It also can only be accomplished if the full costs of exposure, including costs to human health, are quantified (see ref. 55 for a discussion of the costs of other environmental chemicals).

FIFRA places the burden to demonstrate that a pesticide is safe on the manufacturers and registrants. Yet the knowledge gaps that currently exist preclude the drawing of conclusions that GBHs are safe as currently used. FIFRA provides the US EPA with the means to restrict the use of pesticides, to update registered pesticides (like glyphosate) with new safety information, and to take action when new evidence of adverse environmental or human health effects are reported (7 U.S.C. §136 et seq. (1996)). The studies we have outlined in this commentary, together with the burden of proof for safety on the chemical manufacturer, clearly suggests that such actions are needed.


In this commentary, we have identified factors that heighten concerns over the adequacy of safety assessments, and by extension, permitted levels of exposure to glyphosate and GBHs. These factors include increased use of GBHs on crops and for non-crop weed control, leading to measurable concentrations of glyphosate and AMPA in foodstuffs and likely increases in human exposures. The lack of biomonitoring data and epidemiological studies remain important data gaps. A small number of controlled laboratory studies using contemporary scientific approaches have identified adverse effects of glyphosate and GBHs at much lower doses than those used to make risk assessment decisions. Although there is controversy and debate regarding the carcinogenic and endocrine disrupting potential of these compounds, conclusions such as those drawn by IARC call into question the safety of GBHs beyond ‘reasonable certainty of no harm’. Considering what is now known about glyphosate from studies published over the last three decades, as well as the knowledge gaps that continue to raise concerns, we conclude that current safety standards for GBHs are outdated and may fail to protect public health and the environment.

What is already known

  • Glyphosate is a widely used herbicide, and its use continues to rise

  • Epidemiology studies suggest associations between GBH exposures and adverse health outcomes including chronic kidney disease and some cancers

  • A small number of rodent studies suggest that glyphosate can induce cancers

  • The effects of chemical mixtures can be more toxic than the effects of individual compounds

What this study adds

  • We call for improved biomonitoring of glyphosate and its metabolites in human populations

  • We recommend that hazard assessments using state-of-the-art technical approaches be conducted on glyphosate and GBHs

  • Epidemiological studies examining occupationally exposed workers, pesticide manufacturers, and vulnerable populations are needed

  • After review of all evaluations, we conclude that the current safety standards are outdated and fail to protect public health and the environment.


The authors gratefully acknowledge support from the World Federation of Scientists, which funded travel for many of the authors to attend the 48th Session of the International Seminars on Planetary Emergencies and Associated Events, where work on this manuscript was conducted.


Source: BMJ

Hutchinson-Gilford Progeria: Practice Essentials, Background, Pathophysiology

Practice Essentials

Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare hereditary disease that affects the skin, musculoskeletal system, and vasculature. HGPS is characterized by signs of premature aging most notable in the skin, cardiovascular system, and musculoskeletal systems. HGPS is caused by mutations in LMNA that result in the production of an abnormal form of lamin A termed progerin.


The term progeria is derived from the Greek word geras, meaning old age. Significant morbidity and mortality result from accelerated atherosclerosis of the carotid and coronary arteries, leading to premature death during the first or second decade of life. HGPS is considered a segmental aging syndrome, as affected patients do not manifest all of the typical features of aging, such as increased incidence of cancer and neurocognitive decline.

See the image shown below depicting Hutchinson-Gilford progeria syndrome in an infant.

Early Hutchinson-Gilford progeria syndrome. Note t

Early Hutchinson-Gilford progeria syndrome. Note the alopecia, prominent scalp veins, and frontal bossing apparent in this 12-month-old infant with Hutchinson-Gilford progeria syndrome. Midface hypoplasia and micrognathia are less apparent.


Patients with Hutchinson-Gilford progeria syndrome (HGPS) develop clinical features of accelerated aging, including accelerated atherosclerosis of the cerebral and coronary arteries. Unlike arteriosclerosis in the general population, however, in progeria, the only lipid abnormality is decreased high-density lipoprotein cholesterol levels. Interestingly, patients with HGPS do not develop other disease processes associated with aging, such as increased tumor formation, cataract development, or senility. In this sense, HGPS is considered a segmental progeroid syndrome in that it does not recapitulate all of the characteristic phenomena of aging.

Patients with HGPS also develop loss of subcutaneous fat and muscle, skin atrophy, osteoporosis, arthritis, poor growth, and alopecia. There is evidence that patients with HGPS also manifest features of skeletal dysplasia with abnormalities in bone structural geometry and skeletal strength. [6] Extensive lipofuscin deposition, a marker for aging, is extensively distributed in patients with HGPS. Affected organs include the kidneys, brain, adrenal glands, liver, testes, and heart.

 These clinical manifestations occur as the result of defects in processing and function of lamin A, an intermediate filament protein component of the nuclear membrane that regulates a diverse number of cellular functions, including nuclear morphology and integrity, DNA repair, regulation of gene expression, and telomere stability; the end result of these defects is genomic instability, decreased cell proliferation, and premature cell senescence and death. [7] The abnormal protein, progerin, represents a truncated form of the lamin A precursor prelamin A and results from mutations in LMNA. It is interesting to note that mutations in LMNA are associated not only with premature aging syndromes (HPGS, restrictive dermopathy, and atypical Werner syndrome), but also with several muscular dystrophies, lipodystrophic syndromes, and mandibuloacral dysplasia.

Marked loss of vascular smooth muscle cells within the great vessels, arteries, and arterioles associated with sclerosis and fibrosis is a consistent finding in patients with HGPS. [8] Preferential accumulation of progerin in vascular endothelial and smooth muscle cells has been observed. [9]

 Clinically, children with progeria develop atherosclerosis, arteriosclerosis of small vessels, and prominent adventitial fibrosis with increasing deposition of progerin within coronary arteries. [10] The accelerated vascular stiffening and peripheral vascular occlusive disease that develop resemble the cardiovascular features of normal aging and atheroscleroisis. [11] Together with the clinical observations of accelerated and often fatal arteriosclerosis, these findings suggest that the effects of progerin on the cardiovascular system are a major contributor to the pathophysiology of HGPS.
 Interestingly, spontaneous accumulation of progerin has been observed in cultured fibroblasts from normally aged individuals in combination with similar nuclear defects, further reinforcing the theory that HGPS results, at least in part, from accelerated production and accumulation of progerin. [12] It is important to note that the pathophysiology of HGPS results from the presence of progerin and a dominant-negative effect on lamin A function and not simply from the absence of normal lamin A.

International frequency

HGPS is a rare disease with a reported prevalence of 1 in 8 million births. The true prevalence, however, has been suggested to be closer to 1 in 4 million births because many cases likely go undiagnosed or are misdiagnosed. The incidence in the Netherlands over the last century was 1:4,000,000. Approximately 100 cases of HGPS have been reported in the literature.


White persons represent 97% of reported patients. The reason for this racial disparity is unknown.


HGPS has a slight male predilection; the male-to-female ratio is 1.5:1.


Clinical manifestations of HGPS may not be recognized or apparent at birth, although many affected children present with sclerodermatous skin changes. Delayed recognition of the characteristic facial features along with the cutaneous and musculoskeletal manifestations may not occur until age 6-12 months or older, when the development of failure to thrive engenders a more thorough evaluation.


The average life expectancy for a patient with HGPS is 13 years, with an age range of 7-27 years.

 Data from the largest cohort of HGPS patients indicated a mean survival of 14.6 years, with an increased mean survival of 1.6 years in patients treated with a protein farnesylation inhibitor after a median follow-up of 5.3 years from treatment initiation.[13]

Morbidity and mortality in persons with HGPS occur primarily as a result of atherosclerosis of the coronary and cerebrovascular arteries, with at least 90% of patient deaths directly related to complications of progressive atherosclerosis. Cardiovascular complications include myocardial infarction and congestive heart failure. Interstitial fibrosis, diffuse myocardial fibrosis, and calcification of the mitral and aortic valves may occur. Cerebrovascular complications occurring as a result of cerebrovascular infarction include hemiplegia, subdural hematoma, and seizures. Other causes of morbidity and mortality include marasmus, loss of mobility, and inanition.


Evidence of Hutchinson-Gilford progeria syndrome (HGPS) begins within the first 2 years of life. At birth, infants usually appear healthy, although sclerodermatous skin changes have been noted in some patients. Typically, the onset of the disease occurs at age 6-12 months, when skin changes and alopecia are first noted and when the infant fails to gain weight. The following are other suggestive findings [14] :

  • High-pitched voice
  • Short stature and low weight for height, with prenatal onset of growth failure
  • Incomplete sexual maturation
  • Generalized osteoporosis and pathologic fractures
  • Feeding difficulties
  • Delayed dentition, anodontia, hypodontia, or crowding of teeth
  • Low-frequency conductive hearing loss
  • Hypertension
  • Prolonged prothrombin time, elevated platelet counts, and elevated serum phosphorus levels

Emotionally, patients with HGPS share the same feelings as age-matched healthy persons with regard to expressing proper mood and affect. Patients with HGPS are keenly aware of their different appearance and remain reserved in the company of strangers; in the presence of friends, they display affection and good social interaction.

Intelligence is normal.

Physical Examination

The characteristic clinical findings of Hutchinson-Gilford progeria syndrome (HGPS) include abnormalities of the skin and hair in conjunction with characteristic facial features and skeletal abnormalities. [15] The composite appearance of the characteristic facies and parieto-occipital alopecia creates a “plucked-bird” appearance. Evidence of significant growth failure manifests within the first 1-2 years of life and prenatal growth failure is often apparent. [16] The skeletal anomalies are best characterized as a skeletal dysplasia and are thought to be related to microvascular insufficiency and extracellular matrix abnormalities. [16]

Skin and hair findings are as follows:

  • Sclerodermatous skin changes involving the trunk and extremities (see the images below) but sparing the face: These are usually present within the first 6-12 months of life, although they may be present at birth. The skin changes manifest as indurated, shiny, inelastic skin as depicted in the images below. [17]
  • Prominent scalp veins
  • Generalized lipodystrophy with loose, aged-appearing skin: Areas of skin may appear loose, wrinkled, and aged because of the loss of subcutaneous fat, particularly over the hands and feet.
  • Progressive frecklelike hyperpigmentation in sun-exposed areas
  • Hair loss: Scalp hair and eyelashes are progressively lost, resulting in baldness with only a few vellus hairs remaining.

    Sclerodermatous skin changes in Hutchinson-Gilford

    Sclerodermatous skin changes in Hutchinson-Gilford progeria syndrome. This 12-month-old infant with Hutchinson-Gilford progeria syndrome has indurated, shiny skin and mild joint contractures involving the extremities and trunk.

    Sclerodermatous skin changes in Hutchinson-Gilford

    Sclerodermatous skin changes in Hutchinson-Gilford progeria syndrome. This 12-month-old infant has indurated, shiny skin with dyspigmentation.

 Characteristic facies are as follows (see the image shown below):
  • Protruding ears with absent lobes
  • Beaked nose
  • Thin lips with centrofacial cyanosis
  • Prominent eyes
  • Frontal and parietal bossing with pseudohydrocephaly
  • Large anterior fontanel

    Early Hutchinson-Gilford progeria syndrome. Note t

    Early Hutchinson-Gilford progeria syndrome. Note the alopecia, prominent scalp veins, and frontal bossing apparent in this 12-month-old infant with Hutchinson-Gilford progeria syndrome. Midface hypoplasia and micrognathia are less apparent.

Oral and craniofacial anomalies are as follows:

  • Midface hypoplasia with micrognathia
  • Dental anomalies, including hypodontia and delayed dentition [18]
  • Palatal anomalies [18]
  • Stiff auricular cartilage, small or absent lobules, shortened ear canals [19]

Musculoskeletal abnormalities are as follows:

  • Thin limbs with prominent joints
  • Joint contractures and coxa valga with mild flexion of the knees resulting in a wide gait and “horse-riding” stance as depicted in the image below
  • Pyriform (pear-shaped) thorax with short, dystrophic clavicles
  • Bilateral hip dislocations
  • Avascular necrosis of the femoral head

    Enlarged joints, mild flexion contractures, and sc

    Enlarged joints, mild flexion contractures, and sclerodermatous skin changes are seen in this 12-month-old infant with Hutchinson-Gilford progeria syndrome.

Other reported anomalies are as follows:

  • Dystrophic nails
  • Hypertrophic scars
  • Hypoplastic nipples


Hutchinson-Gilford progeria syndrome (HGPS) is related to aberrant processing of the nuclear envelope protein lamin A and accumulation of a farnesylated, truncated prelamin A (progerin). [20]

 Autosomal dominant mutations in the LMNA gene, located on band 1q21.1-1q21.3, are responsible for most cases of HGPS. De novo mutations associated with advanced paternal age are responsible for most cases, although maternal transmission of a mutant LMNA gene from an asymptomatic mother who manifested somatic and gonadal mosaicism has also been reported. In addition, autosomal recessive transmission has also been suggested to account for the reported development of HGPS in several sets of siblings born to unaffected parents.
The LMNA genes encodes the nuclear A-type lamins, which are type V intermediate filament proteins that localize to the cell nucleus and form the nuclear lamina, a structure that supports the nuclear envelope. They are important in maintaining nuclear stability and organizing nuclear chromatin. The nuclear lamins also play a role in regulating gene expression, DNA synthesis, and DNA repair. [21]
The most common LMNA mutation and the one associated with classical HGPS involves a C–>T transition at nucleotide 1824 (G608G). Note the following:
  • This substitution results in the activation of a cryptic splice donor site in exon 11, which results in a 150-base pair deletion and a truncated lamin A protein, called progerin.
  • The abnormal progerin protein acts in a dominant-negative manner to prevent the normal assembly of nuclear lamins into the nuclear lamina.
  • After translation, the mutant preprogerin protein undergoes normal farnesylation of a CAAX tetrapeptide motif located at the carboxyterminus.
  • The farnesylated preprogerin protein is then incorporated into the nuclear membrane. However, the mutant, truncated protein lacks an important posttranslational processing signal required for cleavage of the preprogerin protein at the carboxyterminus. This cleavage is required for the release of prelamin A from the nuclear membrane, thus allowing its incorporation into the nuclear lamina. The abnormal progerin protein forms insoluble cytoplasmic aggregates.
  • As a result of the absence of lamin A in the nuclear lamina, the cell nuclei from HGPS patients display abnormal nuclear blebbing and aberrant nuclear shapes. Abnormal chromosome segregation and delayed onset and progression of mitosis have also been demonstrated. [22, 23]
 The presence of the homozygous missense mutation G1626C (K542N) in LMNAwas demonstrated in 5 siblings born to asymptomatic, consanguineous carrier parents. This study confirms that autosomal recessive inheritance of HGPS can also occur.
Somatic mosaicism for two different LMNA mutations, c.1968+2T>A and c.1968+2T>C, has been described in a child with an intermediate phenotype. [24]

A transgenic mouse model for HGPS has been created by introducing a splicing defect into intron 9 of the mouse LMNA gene. [25] Transgenic mice display many of the features of HGPS, including loss of subcutaneous fat, decreased bone density, growth failure, craniofacial deformities, skeletal abnormalities, and early death.

 Using microarray analyses, 3 recent studies. [26, 27, 28] compared the gene expression profiles of cultured fibroblasts from patients with progeria with those of healthy people of various ages. In general, changes in gene activity detected in older patients correlated with changes in gene activity in progeria patients.

Of the genes expressed differentially in progeria patients, several that help control mitosis were down-regulated. Many genes that control cell division and DNA or RNA synthesis and processing were also shown to be down-regulated in progeria patients; many of these changes are also seen with normal aging. Some of these changes were postulated to lead to genetic instability and a variety of disturbances in gene function.

 Changes were also seen in the expression of many genes involved in collagen remodeling and the formation of the extracellular matrix. In general, the changes favored excess extracellular matrix deposition, which may lead to the characteristic changes seen in the skin and the vasculature in progeria patients. Expression of transforming growth factor-beta, a factor that regulates tissue homeostasis and whose sustained expression is responsible for tissue fibrosis, is highly up-regulated in patients with progeria.
 The expression of several transcription factors, including many involved in musculoskeletal development, were also decreased in progeria patients. Expression of MEOX/GAX, a negative regulator of cell proliferation in mesodermal tissue, is elevated almost 30-fold in patients with HGPS, suggesting a contributory role in the development of the musculoskeletal abnormalities seen in HGPS.
 A characteristic finding in persons with progeria is an increase in hyaluronic acid excretion. In addition to persons with progeria, it is only detected in those with Werner syndrome, a disease characterized by a later onset of premature aging that occurs during the second decade of life.
 Usually, hyaluronic acid and other glycosaminoglycan production increases during the fifth to seventh decades of life. Possibly, the increase in hyaluronic acid is a normal feature of advancing age. Fibroblasts from patients with progeria show a 3-fold increase in total glycosaminoglycan production and, in particular, hyaluronic acid production, compared with age-matched control groups. This increase results from an abnormality in degradation and is not caused by increased synthesis.

Data from embryonic development suggest that changes in the level of hyaluronic acid are extremely important for morphological development. Experiments performed in chick embryos have demonstrated a correlation between cell differentiation and hyaluronic acid degradation. Hyaluronic acid is also necessary for the morphologic development of blood vessels in chick embryos. A reduction or absence of blood vessels is noted in regions of high hyaluronic acid levels. The decreased density of vasculature, sclerodermatous changes in the skin, and the high prevalence of cardiovascular disease present in persons with progeria may be induced by increased hyaluronic acid levels. Increased hyaluronic acid levels may also promote calcification of blood vessels, thus contributing to arteriosclerosis.

In the past, studies of the link between progeria and aging (among other topics) have investigated the role of fibroblast life span.

 Cells from older donors exhibit a reduced number of cell divisions in comparison to younger donor cells. The reduction of life span in cultured fibroblasts derived from patients with progeria has revealed inconsistent results. A significant reduction in fibroblast life span has been claimed in some studies but has been questioned in later investigations. A recent thorough study indicates the life span of fibroblasts in culture is independent of donor age.

Further abnormalities observed in cultured fibroblasts from patients with progeria include reduced mitotic activity, DNA synthesis, and cloning efficiency and a reduced capacity for DNA repair in cultured progeria fibroblasts after gamma irradiation. Mutant fibroblasts have been shown to demonstrate impaired DNA damage checkpoint signaling, which results in increased DNA double-strand breaks. [29]


Death due to cardiovascular abnormalities occurs in approximately 75% of HGPS patients. Other causes of death mentioned in the literature include stroke, marasmus, inanition, seizures, and accidental head trauma.

Diagnostic Considerations

Werner syndrome (pangeria) findings are as follows:

  • Onset age of 15-30 years
  • Prematurely aged appearance
  • High-pitched voice
  • Beak-shaped nose
  • Sclerodermatous skin
  • Immature sexual development
  • Cataracts
  • Hypogonadism
  • Arteriosclerosis: Complications of arteriosclerosis reduce life expectancy to the fifth decade.
  • RECQL2 (a DNA helicase gene) mutations

Acrogeria (Gottron type) findings are as follows:

  • Onset occurring up to age 6 years
  • Premature aging of extremities
  • Cutaneous atrophy and subcutaneous wasting of the face and extremities
  • Hair unaffected
  • No atherosclerosis or systemic disease

Rothmund-Thomson syndrome findings are as follows:

  • Onset age of 3-6 months
  • Cataracts
  • Poikilodermatous skin changes
  • Premature graying of the hair and/or alopecia
  • Increased photosensitivity
  • Short stature
  • Microcephaly
  • Hypogonadism
  • RECQL4 (a DNA helicase) mutations

Cockayne syndrome findings are as follows:

  • Onset during second year of life
  • Marked loss of subcutaneous fat
  • Growth failure
  • Increased photosensitivity
  • Ocular abnormalities (eg, optic atrophy, pigmentary retinopathy)
  • Microcephaly
  • Ataxia and progressive mental deterioration
  • Disproportionally large hands and feet
  • Protruding ears
  • Sensorineural hearing loss

Seckel syndrome findings are as follows:

  • “Bird-head” facies
  • Dwarfism
  • Trident hands
  • Skeletal defects
  • Hypodontia
  • Hypersplenism
  • Premature graying
  • Stiff skin syndrome
  • Diffuse progressive hardening of the skin, usually starting in the gluteal region, beginning at birth or early infancy
  • Joint contractures
  • Hypertrichosis
  • Hyperpigmentation
  • Increased cutaneous (but not systemic) mucopolysaccharide levels
  • In the autosomal recessive Paraná type, severe growth retardation and respiratory insufficiency leading to early death
  • Congenital fascial dystrophy
  • Diffuse, progressive hardening of the skin, usually starting in the gluteal region, beginning at birth or early infancy
  • Joint contractures
  • No systemic disease
  • Histologically, abnormally thickened fascia along with giant amianthoidlike fibrils and myofibroblasts
  • Restrictive dermopathy
  • Profound intrauterine growth retardation
  • Severe arthrogryposis (joint contractures)
  • Diffuse skin hardening
  • Pulmonary hypoplasia
  • Characteristic facies
  • Lethal in neonatal period
  • LMNA or ZMPSTE24 mutations

Wiedemann-Rautenstrauch syndrome findings are as follows [30] :

  • Onset at birth
  • Pseudohydrocephalus with wide sutures
  • Triangular facies
  • Aged appearance
  • Growth retardation
  • Generalized lack of subcutaneous fat
  • Prominent scalp veins
  • Sparse hair

DeBarsy syndrome findings are as follows:

  • Onset at birth
  • Aged appearance
  • Joint laxity
  • Loose, wrinkled skin
  • Hypotonia
  • Developmental delay
  • Ocular abnormalities (eg, strabismus, cataracts, myopia)

Berardinelli-Seip syndrome findings are as follows:

  • Onset at birth
  • Decreased subcutaneous fat/lipodystrophy
  • Pseudohypertrophy of muscles
  • Acanthosis nigricans
  • Hyperinsulinemia
  • Acromegaloid appearance
  • Hypertriglyceridemia

Donahue syndrome (leprechaunism) findings are as follows:

  • Onset at birth
  • Elfin facies
  • Hyperinsulinemia
  • Failure to thrive
  • Hypertrichosis
  • Acanthosis nigricans
  • Decreased subcutaneous fat
  • Loose skin
  • Prominent nipples
  • Insulin receptor gene mutation

GAPO (growth retardation, alopecia, pseudoanodontia, optic atrophy) syndrome findings are as follows:

  • Onset age of 1-2 years
  • Growth retardation
  • Alopecia
  • Pseudoanodontia
  • Optic atrophy
  • Craniofacial dysmorphism
  • Coarse facies
  • Aged appearance
  • Joint laxity
  • Loose skin

Hallermann-Streiff syndrome findings are as follows:

  • Onset at birth
  • Brachycephaly
  • Mandibular hypoplasia
  • Beaked nose
  • Alopecia
  • Cutaneous atrophy of the face and scalp
  • Ocular abnormalities (eg, cataracts, nystagmus, microphthalmos)
  • Dental anomalies

Familial mandibuloacral dysplasia findings are as follows:

  • Onset age of 3-5 years
  • Alopecia
  • Beaked nose
  • Premature loss of teeth
  • Acroosteolysis
  • Dysplastic clavicles
  • Atrophy of extremity skin
  • Mandibular hypoplasia
  • Delayed cranial suture closure
  • LMNA mutations

Differential Diagnoses

Laboratory Studies

Abnormalities in serum lipid levels are limited to low high-density lipoprotein levels, which are associated with atherosclerotic disease. Serum low-density lipoprotein and total cholesterol levels are normal in patients with Hutchinson-Gilford progeria syndrome (HGPS).

Elevated levels of hyaluronic acid excretion are seen in the urine of patients with HGPS but are not diagnostic. The significance is unknown.

Imaging Studies

Radiography findings usually begin to manifest within the first or second year of life and most commonly involve the skull, thorax, long bones, and phalanges. [16, 31]Typical findings are as follows:

  • Generalized osteopenia
  • Acroosteolysis (distal bone resorption) of the phalanges and distal clavicles
  • Pseudoarthrosis of the distal clavicle
  • “Fish-mouth” vertebral bodies
  • Coxa valga and hip dysplasia
  • Attenuated cortical bone
  • Widened metaphyses, epiphyseal overgrowth, and narrow diaphyses
  • Avascular necrosis of the femoral head
  • Focal concave cortical defects at or near to the insertion of a major muscle group
  • Dystrophic calcification, typically distal to the tufts of the fingers
  • Normal bone age
 Use of CT and MRI has identified a spectrum of craniofacial structural bone and soft tissue abnormalities. [32] Common craniofacial abnormalities seen in progeria include the following:
  • J-shaped sella
  • Increased calvarial vascular markings
  • Abnormal mandibular condyles
  • Hypoplastic articular eminences
  • Small zygomatic arches
  • Prominent parotid glands
  • Optic nerve kinking

Brain magnetic resonance angiography may identify cerebrovascular occlusive disease. Features of a distinct vasculopathy may be seen, including intracranial steno-occlusive arterial lesions, basal cistern collateral vessels, and slow compensatory collateral flow over the cerebral convexities; vertebral artery stenosis with stenosis and calcification of both the cervical internal and common carotid arteries; and high percentage of both early symptomatic and clinically silent infarcts.

Other Tests

Serial ECG and echocardiography should be performed to monitor for coronary artery disease and congestive heart failure.

Histologic Findings

Skin biopsy specimens from firm, sclerotic areas reveal the characteristics of scleroderma.

 In the early stages, the epidermis appears moderately acanthotic with some effacement of the rete ridges. Thickened collagen bundles may be seen in the dermis. Progressive deposition of thickened, homogenized collagen that extends into the subcutaneous tissue is observed. In the upper dermis, a mild perivascular infiltrate may be observed. The amount of acid mucopolysaccharides is increased.
 At later stages, the subcutaneous fat is greatly reduced, except for some sparse fat lobules surrounded by connective tissue. Hyalinized dermal collagen is prominent. Blood vessels exhibit a moderate thickening of the muscle wall with a narrowing of the vascular lumen. Hair follicles may appear atrophic.

Approach Considerations

Pharmacologic approaches to the treatment of Hutchinson-Gilford progeria syndrome (HGPS) may involve attempts to reduce the expression or accumulation of progerin and promote autophagy.

Medical Care

To date, there is no approved therapy for HGPS.

 In vitro, exposure of cultured HGPS fibroblasts to rapamycin, a macrolide antibiotic that has been shown to regulate aging-related cellular pathways, and its analog temsirolimus, has been demonstrated to prevent or reverse nuclear blebbing, retard cellular senescence, enhance autophagic degradation of progerin, and delay the development of cellular senescence, suggesting that it may be a useful therapy for children with progeria. [34, 35, 36, 37, 38] The addition of all-trans retinoic acid to low-dose rapamycin reduces the expression of progerin and prelamin A in cultured fibroblasts and suggests an additional pharmacologic treatment for progeria. [39]
Careful monitoring for cardiovascular and cerebrovascular disease is essential. The use of low-dose aspirin is recommended as prophylaxis against cardiovascular and cerebrovascular atherosclerotic disease.

Physical and occupational therapy can help to maintain physical activity and an active lifestyle. The use of hydrotherapy may be particularly effective in improving joint mobility and minimizing symptoms of arthritis.

 Infants with HGPS may exhibit poor feeding. Provision of adequate nutritional intake may require placement of a gastrostomy tube for supplemental enteral feeding. In older children, the daily consumption of high-energy supplements is recommended, along with careful monitoring of growth and nutrition.

The use of growth hormone has been used to decrease catabolic demands and augment weight gain and linear growth in a small number of patients with progeria.[40]

 Sulforaphane, an antioxidant derived from cruciferous vegetables, has been demonstrated to stimulate proteasome activity and autophagy in cultured HGPS fibroblasts, to enhance progerin clearance by autophagy, and to restore a normal cellular phenotype. [41]
In vitro studies also suggest a possible role for the use of farnesyltransferase inhibitors (FTIs) in HGPS. [42] FTIs appear to promote the release of the mutant prelamin A (preprogerin) from the nuclear membrane, allowing it to be correctly incorporated into the nuclear lamina, thus correcting the structural and functional nuclear defects, although it remains to be determined whether use of FTIs also has an effect on the abnormalities seen in HGPS that result from loss of normal lamin A function.

In vivo studies using FTIs in transgenic mouse models have demonstrated encouraging results with regards to prevention of the cardiovascular complications seen in progeria [43] as well as reversal of the cutaneous manifestations [44] and overall improvement in many of the phenotypic features of progeria, including increased longevity. [45, 46]

 Treatment of transgenic mice expressing progerin in the epidermis with FTI-276, a farnesyltransferase inhibitor, or a combination of pravastatin, a lipid-lowering agent, and zoledronic acid, an agent used to increase bone mineral density, has been shown to reverse the morphological nuclear abnormalities that are seen in HGPS.[47]

Results from a clinical trial of lonafarnib, an FTI, in progeria have indicated that treatment with lonafarnib may improve weight gain, increase bone mineral density, reduce vascular stiffness, and result in improved sensorineural hearing in patients with progeria. [48] Lonafarnib treatment has also been shown to reduce the frequency of clinical stroke, headaches, and seizures. [49]

 Results from a clinical trial that combined use of lonafarnib with two additional protein farnesylation inhibitors, pravastatin and zoledronic acid, demonstrated increased bone mineral density without any additional cardiovascular benefit as compared with lonafarnib monotherapy. [50]

Preliminary in vitro studies using transfection of modified oligonucleotides that target the cryptic splice site that occurs in patients with the common 1824C–>T mutation have also produced encouraging results. Transfection of an exon 11 antisense oligonucleotide reduced lamin A expression in wild-type mice and progerin expression in an HGPS mouse model. [51] By eliminating the production of the mutant LMNA mRNA and protein, normal nuclear morphology is restored, with resultant normalization of heterochromatin structure and gene expression. These nascent studies provide early support for the rationalization of genetic therapy for HGPS patients.

 In vitro, use of rapamycin, a macrolide antibiotic, and its analog temsirolimus, has been demonstrated to prevent nuclear blebbing, enhance autophagic degradation of progerin, and delay the development of cellular senescence, suggesting that it may be a useful therapy for children with progeria. [34, 35, 36, 37, 38]
 Patients, families, and physicians may obtain further information, including opportunities for possible enrollment in clinical trials, through the Progeria Research Foundation.


Appropriate care for children with HGPS requires coordinated care from several specialists.

 Pediatric cardiologists provide regular assessment of cardiovascular status, including monitoring and treatment for early atherogenic cardiac disease.

Physical and occupational therapists can develop individualized physical therapy programs to help to maintain physical activity, coordination, and flexibility.

 Dermatologists and/or geneticists may be the first specialists to evaluate an infant with suspected HGPS and can perform diagnostic testing, including genetic mutation analysis and skin biopsies, as needed.

Pediatric gastroenterologists, feeding therapists, and nutritionists can aid in diagnosing and treating feeding disorders and failure to thrive.

 Pediatric dentists with experience in treating children with dental anomalies can be helpful. Routine fluoride supplementation should be provided to minimize the risks of dental caries. Regular, gentle dental care minimizes the development of periodontal disease.


Infants and children with HGPS may experience feeding difficulties and failure to thrive. The use of age-appropriate nutritional supplements is recommended.


Children with HGPS do not require activity restrictions. With adequate supervision, most children are able to experience a wide range of physical activities.

Guidelines Summary

There are currently no peer-reviewed clinical guidelines for the management of Hutchinson-Gilford progeria.

The Progeria Research Foundation published The Progeria Handbook for parents and clinicians in 2010. It is available through the Progeria Research Foundation.



Monsanto Dicamba Herbicide

Help Support Organics and the Battle Against GMOs

GMO proponents claim that genetic engineering is “safe and beneficial,” and that it advances the agricultural industry. They also say that GMOs, or genetically “engineered” (GE) foods, help ensure the global food supply and sustainability. But is there any truth to these claims? I believe not. For years, I’ve stated the belief that GMOs pose one of the greatest threats to life on the planet. Genetic engineering is NOT the safe and beneficial technology that it is touted to be.

The FDA cleared the way for GE (Genetically Engineered) Atlantic salmon to be farmed for human consumption. Thanks to added language in the federal spending bill, the product will require special labeling so at least consumers will have the ability to identify the GE salmon in stores. However, it’s imperative ALL GE foods be labeled, which is currently still being denied.

The FDA is threatening the existence of our food supply. We have to start taking action now. I urge you to share this article with friends and family. If we act together, we can make a difference and put an end to the absurdity. Thankfully, we have organizations like the Organic Consumers Association (OCA) to fight back against these corporate giants. So please, fight for your right to know what’s in your food and help support the GMO labeling movement by making a donation today.

Donations TRIPLE-Matched During GMO Awareness Week

I have found very few organizations that are as effective and efficient as OCA. It’s a public interest organization dedicated to promoting health and sustainability. OCA and I thank you for everything you’ve done to further this cause, and hope you stick with us as we move forward. I strongly encourage you to give OCA your financial support, because we are making a huge difference.

Food companies have to start being honest and truthful in telling us what’s in our food, and we will not quit until they do. We can’t do it alone, however. We need your help, and this week, you can seriously maximize the impact of your generosity, because I will match each and every dollar you donate to the OCA with $3, up to $250,000.

Watch the video. URL:

How GMO Crops Impact Livestock and Human Health Worldwide

Help Support Organics and the Battle Against GMOs

GMO proponents claim that genetic engineering is “safe and beneficial,” and that it advances the agricultural industry. They also say that GMOs, or genetically “engineered” (GE) foods, help ensure the global food supply and sustainability. But is there any truth to these claims? I believe not. For years, I’ve stated the belief that GMOs pose one of the greatest threats to life on the planet. Genetic engineering is NOT the safe and beneficial technology that it is touted to be.

The FDA cleared the way for GE (Genetically Engineered) Atlantic salmon to be farmed for human consumption. Thanks to added language in the federal spending bill, the product will require special labeling so at least consumers will have the ability to identify the GE salmon in stores. However, it’s imperative ALL GE foods be labeled, which is currently still being denied.

The FDA is threatening the existence of our food supply. We have to start taking action now. I urge you to share this article with friends and family. If we act together, we can make a difference and put an end to the absurdity. Thankfully, we have organizations like the Organic Consumers Association (OCA) to fight back against these corporate giants. So please, fight for your right to know what’s in your food and help support the GMO labeling movement by making a donation today.

Donations TRIPLE-Matched During GMO Awareness Week

I have found very few organizations that are as effective and efficient as OCA. It’s a public interest organization dedicated to promoting health and sustainability. OCA and I thank you for everything you’ve done to further this cause, and hope you stick with us as we move forward. I strongly encourage you to give OCA your financial support, because we are making a huge difference.

Food companies have to start being honest and truthful in telling us what’s in our food, and we will not quit until they do. We can’t do it alone, however. We need your help, and this week, you can seriously maximize the impact of your generosity, because I will match each and every dollar you donate to the OCA with $3, up to $250,000.

Watch the video. URL:

The Ultimate Guide to GMO Foods eBook –

Discover the Truth About GMO Foods – Get The Ultimate Guide to GMOs eBook for Free!

Due to the prevalence of GMO foods in the food industry, Dr. Mercola shares everything you need to know about these deceptive foods in his free eBook, The Ultimate Guide to GMOs.

You also get free access to more than 100,000 health articles from and FREE subscription to my Natural Health newsletter! You can unsubscribe any time and I guarantee your email privacy.

 Spare Yourself from Being Fooled by GMO Foods – Learn the Truth Behind GM Crops

With the advent of technology, scientists are continuously discovering methods to advance our food system. They’ve come up with outrageous ways of altering our food supply, and one of those is through the invention of GMO foods.

As the curiosity and concern of many people grow, they are now starting to ask: what is a GMO food?

GMO foods or genetically modified organisms are produced from the unusual combination and alteration of any organism’s genetic components. Once the seeds of any crop have been genetically engineered or modified, it promises to make every farmer’s dream to come true.

The big biotech companies that produce GMOs guarantee that GM crops or seeds will result in abundant harvest and less use of pesticides and herbicides. They also said that foods produced from GMO crops are generally safe and can sustain global food supply.

But do GMOs live up to their promise? Are GMO foods really the answer to solving hunger around the world?

Find out the truth and repercussions brought by GMOs in our food industry with my free eBook, The Ultimate Guide to GMOs. In it, I will share to you my discoveries about the dangers lurking behind the use of GM crops.

Are You Serving Genetically Modified Foods to Your Family?

If you’re a complacent shopper, you might be picking whatever food is on the grocery shelf. You might be perfectly satisfied that the food industry is giving you the food, thinking that it’s got your best interests in mind.

But you’re certainly wrong – all they have in mind is how much profit genetically modified foods will bring into their pockets.

Some of the most cultivated GM crops today include:

  • GM corn. Monsanto’s Bt corn produces its own pesticide that kills insects. About 85 percent of corns planted in the country are genetically modified.
  • GM soybean. It is estimated that 91 percent of soybeans currently available are genetically engineered.
  • GM cotton. About 88 percent of the cotton industry has been genetically engineered to produce its own pesticide.

Aside from these, there are many other crops and seeds that are genetically engineered. And you might be purchasing them unknowingly. Learn more about them in my latest eBook, The Ultimate Guide to GMOs, where I reveal various genetically modified foods that you must veer away from.

Support GMO Labeling and Know What You Are Eating

More than 80 percent of processed foods today contain genetically engineered ingredients. Despite the fact that genetically modified foods are now widely prevalent in the food industry, consumers like you can still do something to change its course by carefully choosing and buying organic foods.

That’s what GMO labeling is all about. GMO labeling aims to give you the freedom to choose the food you’re buying. It is very important that consumers are given the right to know if the food they’re purchasing contains genetically engineered ingredients.

However, there are many forces who greatly oppose GMO labeling — giant food and biotech businesses that are willing to shell out huge amounts of cash just to continue and ensure that they still reign over the grocery shelves. Read my FREE eBook,The Ultimate Guide to GMOs, and you will be surprised to know who are the companies who are willing to put you at risk in exchange for profits.

Educate yourself and your loved ones on the nitty-gritty about GMOs. Discover which foods are truly healthy for you and get rid of the ones that are slowly destroying your body. Read this eBook today!

The Ultimate Guide to GMOs

Discover the Truth About GMO Foods – Get The Ultimate Guide to GMOs eBook for Free!

Due to the prevalence of GMO foods in the food industry, Dr. Mercola shares everything you need to know about these deceptive foods in his free eBook, The Ultimate Guide to GMOs.


Just enter your email address below. You’ll also receive Dr. Mercola’s health newsletter for FREE.


 What People Are Saying About the Natural Health Newsletter

Should we screen extensively for cancer after unprovoked venous thrombosis?

What you need to know

  • The prevalence of occult cancer in patients with a first unprovoked venous thromboembolism seems to be lower (~4%) than previously reported (10%)

  • There is limited evidence to recommend extensive cancer screening with computed tomography in such patients

  • Consider history and physical examination, basic laboratory tests, and results from routine age-specific cancer screening to guide further testing as an alternative to extensive screening

How far to go in screening patients with an unprovoked venous thromboembolism (VTE) for an occult cancer is a clinical dilemma. Unprovoked VTE, either deep vein thrombosis or pulmonary embolism, can be the first manifestation of an undiagnosed cancer. Until recently, the literature suggested that up to 10% of such patients would be diagnosed with a cancer in the year after their diagnosis of VTE.1 However, the incidence of occult cancer in patients studied in two recent, high quality, randomised controlled trials was only about 4%.23 This drop in the proportion of people with occult cancer may require an adjustment in the clinical approach.

Fig 1⇓ outlines a conservative approach and a more detailed approach to investigating such patients. Extensive screening has become the standard of care, though it is based on limited data.

 However, high quality data from recently completed trials discussed below suggest that extensive screening strategies may not provide additional value over routine cancer screening in the frequency of cancer detection in these patients.

What is the evidence of uncertainty?

Search strategy and study selection

We searched PubMed (from inception to 31 December 2016) for randomised controlled trials and systematic reviews using the search terms “cancer screening,” “venous thromboembolism,” “unprovoked,” “meta-analysis,” and “randomized controlled trial.” We reviewed articles published in English between 2012 (publication of NICE guidelines) and 2016.


Hidden Dangerous Sushi Ingredients Exposed


Story at-a-glance

  • Popular ingredients in sushi and other Asian foods often contain monosodium glutamate (MSG), artificial sweeteners, high-fructose corn syrup, genetically modified ingredients, artificial colors, and artificial flavors
  • Seaweed salad, pickled ginger, wasabi, soy sauce, and even sushi rice and sesame seeds may contain artificial ingredients and additives
  • Restaurant sushi is often mislabeled and may include a different fish than is labeled; it also may be high in mercury or other pollutants
  • If you love sushi, try making it at home by purchasing a whole, pollutant-free fish, such as wild-caught, Alaskan sockeye salmon

Most people regard sushi as a healthful choice when eating out, or even when looking for a quick take-out option, as ready-made sushi is now widely available in grocery stores.

Obviously, if you order certain sushi rolls that are deep-fried, you’re probably already aware that not everything on the menu at your favorite Asian restaurant is actually healthy.

But what may come as a surprise – even to the most health-conscious sushi lovers – are the potentially dangerous ingredients hidden in even seemingly excellent choices – like seaweed salad, wasabi, or sushi ginger.

Dangerous Ingredients Lurking in 8 Popular Sushi Dishes

A revealing report1 by Andrea Donsky, founder of NaturallySavvy, has exposed the many not-so-healthy ingredients found in popular Asian foods.

1. Seaweed Salad

Seaweed is an excellent source of iodine, vitamins, and minerals, provided it comes from clean, non-polluted waters. But the seaweed salad sold at many sushi restaurants comes pre-made in bulk from distribution companies and may contain:

  • High-fructose corn syrup
  • Vegetable oil
  • Hydrolyzed protein (which contains monosodium glutamate or MSG)
  • Artificial color, such as yellow #4 and blue #1
  • Genetically modified (GM) ingredients

A fairly surefire sign that your favorite sushi salad contains some of these “pre-packaged” ingredients is an unnaturally bright green color. You can also ask the restaurant directly if it makes its own seaweed salad.

2. Ginger

Ginger has phenomenal health benefits for conditions ranging from nausea and arthritis pain to heart health and asthma. Unfortunately, the pickled ginger often served alongside sushi is often doctored-up with some dangerous additives, including:

  • Monosodium glutamate
  • Aspartame
  • Potassium sorbate (a preservative)
  • Artificial colors, including red #40, which is linked to hyperactivity in children (if the ginger looks pink)

3. Wasabi

The bright green Japanese mustard known as wasabi has anti-inflammatory, anti-microbial, anti-platelet, and, potentially, anti-cancer effects. However, this is referring to authentic wasabi (the kind that comes from the wasabia japonica root or rhizome).

Authentic wasabi is extremely hard to come by, even in Japan, and it’s estimated that only 5 percent of restaurants in Japan and only very high-end restaurants in the US2serve the real deal. So what is that green paste being served with your sushi? Most likely a combination of horseradish, Chinese mustard, and green food coloring. The featured report found the following in wasabi:

  • Artificial flavors
  • Artificial colors
  • Potential GM ingredients (corn and soy)

A better alternative is to look for “wasabi” that’s made from only horseradish, spirulina, and turmeric, which is likely to be far healthier than the wasabi imposters being sold at most sushi restaurants.

4. Sesame Seeds

That’s right… even sesame seeds may contain hidden ingredients! While most sushi restaurants use plain toasted sesame seeds in their dishes, there are some flavored sesame seeds on the market that also contain:

  • Artificial colors
  • Artificial sweeteners (sucralose)

5. Soy Sauce

The soy sauce served alongside your sushi also likely contains additives you’re far better off avoiding, including:

  • Hydrolyzed soy protein (MSG)
  • GM ingredients (soy and con)
  • Corn syrup
  • Potassium sorbate (preservative)
  • Caramel color (certain types of which may form potentially carcinogenic byproducts)

6. Rice

The rice used on sushi rolls may also contain hidden ingredients used to make it sweeter. The featured report revealed sushi rice may contain:

7. Imitation Crab

Imitation crab meat may be made from Golden Threadfin Bream, a fish facing extinction, and that’s not all. It may also contain additives including:

  • Monosodium glutamate
  • Artificial flavor

8. Fish Roe (Seasoned Caviar)

The orange-colored fish eggs often served with sushi dishes are also commonly full of additives like those found in other Asian foods. Among them:

  • Monosodium glutamate
  • High-fructose corn syrup
  • Artificial color (yellow #6)

Tuna and Snapper Sushi Are Probably Not What You Think

When you factor in all of the additives found in many sushi dishes, it becomes clear that this potentially healthful food has succumbed to the processed food trap of artificial additives and fillers in lieu of real, quality ingredients. But there is more to the story than even this… When you eat tuna at your favorite sushi restaurant, there’s a good chance you’re not actually eating tuna. Instead, the majority of fish labeled “white tuna” may actually be escolar, a type of fish that can cause serious digestive effects, including oily anal leakage.

Oceana conducted DNA testing on more than 1,200 fish samples across the US and found that one-third were mislabeled.3 While red snapper had the highest mislabeling rates (87 percent of “red snapper” samples were not actually red snapper), tuna was a close second, with 59 percent mislabeled.

At sushi restaurants, however, 74 percent of fish samples were mislabeled. This included every single sushi restaurant from which samples were tested, even in major metropolitan areas like Chicago, Austin, New York and Washington DC. In many cases, the mislabeled fish had been substituted for cheaper, less desirable and/or more readily available fish varieties. More than 90 percent of the seafood consumed in the US is imported, yet only 1 percent of imports are inspected for fraud, which may explain this clearly out-of-control situation.

Sushi Tuna Is Typically High in Mercury

Most major waterways in the world are contaminated with mercury, heavy metals, and chemicals like dioxins, PCBs, and other agricultural chemicals that wind up in the environment. Fish has always been the best source for the animal-based omega-3 fats EPA and DHA, but as levels of pollution have increased, this health treasure of a food has become less and less viable as a primary source of beneficial fats.

This is particularly true for tuna, which tends to be a higher mercury fish. One study from the U.S. Geological Survey found that ALL tuna tested contained fairly high amounts of mercury. The contamination may be even worse in restaurants, again confirming that eating restaurant tuna is a risky proposition.

Further, according to a separate study, toxicological testing revealed that tuna sold in restaurants actually contained higheramounts of mercury than the store-bought variety.4 The reason is that restaurants tend to favor certain species of tuna, such as bluefin akami and bigeye tuna, which had significantly higher levels of mercury than bluefin toro and yellowfin tuna. Unfortunately, mercury tends to accumulate to a greater degree in muscle than in fat, rendering these highly prized, leaner species of tuna more susceptible to high contamination.

Can You Still Enjoy the Sushi You Love?

If you love sushi, and want to enjoy it without adding unnecessary health risks, try making it at home. You can purchase a whole, low-mercury fish, such as wild-caught Alaskan sockeye salmon, and use natural versions of ginger and wasabi for condiments. If this sounds daunting, there are many tutorials on how to make your own sushi simply at home available online.

Additionally, whenever I consume fish, I make sure to also take chlorella tablets. The chlorella is a potent mercury binder and, if taken with the fish, will help bind the mercury before you are able to absorb it, so it can be safely excreted in your stool.

If you want to eat out, search around for a higher end restaurant that makes its own dishes, like seaweed salad, and will be upfront about disclosing ingredients. Steer clear of tuna due to its mercury content in favor of lower mercury wild-caught salmon, and consider bringing your own natural versions of wasabi or pickled ginger (available in some health food stores) from home. You can also try some of the all-vegetable options and forgo the seafood entirely, if you’re in doubt about its variety or purity.

Be sure to avoid any sushi made from farmed fish. Remember, fish farms are the aquatic version of a concentrated animal feeding operation (CAFO), and just like land-based cattle and chicken farms, fish farms breed disease due to crowding too many fish together in a small space. They also produce toxic waste, and fish of inferior quality. These fish are further contaminated by drugs and genetically modified corn and soy meal feed, and in the case of salmon, synthetic astaxanthin, which is made from petrochemicals that are not approved for human consumption.

11 Vegetables Anyone Can Grow on Their Own

Growing Vegetables

Story at-a-glance

  • One in three US households are now growing food
  • Some of the easiest vegetables for beginner gardeners to grow include cherry tomatoes, cucumbers, carrots, chard, kale, and herbs
  • If you don’t have space in your backyard for a garden, you can grow vegetables in containers on your patio, balcony, rooftop, or windowsill

One in three US households are now growing food, according to a special report from the National Gardening Association (NGA).1 This equates to about 42 million households with a food garden in 2013, a 17 percent increase from 2008.

Keeping a garden can improve your health by providing you with fresher, uncontaminated food, and cutting your grocery bill. NGA estimates that while the average US family spends $70 per year to plant a vegetable garden, they grow about $600 worth of produce – that’s a $530 return on your investment.2

The promise of garden-fresh tomatoes, cucumbers, sweet peppers, and carrots is what initially draws many new gardeners in… but what keeps many involved is the intrinsically rewarding feeling of growing your own food.

11 Foods That Are Easy to Grow at Home

You might be surprised at how much food you can grow from just a few packets of seeds. Even if you’re new to gardening, many of the foods that follow are relatively foolproof options that will deliver a robust harvest, sometimes in as little as a few weeks from planting.3

Keep in mind that even if you don’t have space in your backyard for a garden, you can grow vegetables in containers on your patio, balcony, or rooftop. Community gardens are also growing in popularity where you can rent a plot of soil to grow food for your family.

If this is your first garden, you might want to start out with just a few options from this list. You’ll probably need to experiment with different methods of planting, watering, building soil health, and controlling pests naturally, but as you gain confidence, and harvest the fruits of your labor, your garden (and your passion for gardening) will likely continue to grow.

If you’re not sure of which seeds to choose, check out my Heirloom Seed Kits for wonderful selections of vegetables, fruits, herbs, and flowers that are non-hybrid, non-GMO, non-treated, and non-patented, in selections for both Northern and Southern climates.

1. Sprouts

Growing your own sprouts is quite easy, and you don’t need a whole lot of space either; they can even be grown indoors. Sprouts may be small, but they are packed with nutrition, including vitamins, minerals, antioxidants, and enzymes that help protect against free radical damage.

Two of my personal favorites are sunflower seed and pea shoots—both of which are typically about 30 times more nutritious than organic vegetables. They’re also among the highest in protein. In addition, sunflower seeds contain healthy fats, essential fatty acids, and fiber—all of which are important for optimal health.

I used Ball jars when I first started sprouting seeds about 25 years ago, but I’ve since switched over to growing them in potting soil. With Ball jars you need to rinse them several times a day to prevent mold growth and it is a hassle to have them draining in the sink, taking up space.

Moreover, you need dozens of jars to produce the same amount of sprouts as just one flat tray. I didn’t have the time or patience for that, and you may not either. The choice is yours though. You can easily grow sprouts and shoots with or without soil.

My Sprout Doctor Starter Kit comes with what I consider to be three of the best sprouts to grow – sunflower shoots, broccoli sprouts, and pea shoots. When grown in soil, you can harvest your sprouts in about a week, and a pound of seeds will probably produce over 10 pounds of sprouts.

Sunflower shoots will give you the most volume for your effort and, in my opinion, have the best taste. In one 10×10 tray, you can harvest between one and two pounds of sunflower sprouts, which will last you about three days. You can store them in the fridge for about a week. Broccoli sprouts look and taste similar to alfalfa sprouts, which most people like.

They’re perfect for adding to salads, either in addition to or in lieu of salad greens, and sandwiches and are especially tasty in combination with fresh avocado. You can also add them to your vegetable juice or smoothies.

I’ve partnered with a company in a small town in Vermont that develops, breeds, and grows their own seeds, and is an industry leader in seed safety for sprouts and shoots.

All of my seeds are non-GMO, certified organic, and packed with nutrition. My starter kit makes it easy to grow your own sprouts in the comfort of your home, whenever you want. It provides everything you need, so all you have to do is grow and enjoy your sprouts.

2. Spinach and Loose-Leaf Lettuce

Early spring is a good time to plant spinach and other loose-leaf greens. The harvest is ready in just three to five weeks; simply cut off leaves here and there with scissors (don’t worry, they’ll grow back). Up to half of the nutrients in lettuce may be lost within two days of harvest, so growing your owns leads to a much more nutritious salad.

3. Kale

One cup of kale contains just around 30 calories but will provide you with seven times the daily recommended amount of vitamin K1, twice the amount of vitamin A and a day’s worth of vitamin C, plus antioxidants, minerals, and much more.

This leafy green also has anti-inflammatory properties that may help prevent arthritis, heart disease, and autoimmune diseases – plant-based omega-3 fats for building cell membranes, cancer-fighting sulforaphane, and indole-3-carbinol, and an impressive number of beneficial flavonoids.

Kale grows all season long, but its flavor gets sweeter after a frost. Impressively, kale can survive temperatures as low as 10° Fahrenheit, so be sure to keep it growing into the fall and winter. Kale is ready to harvest about a month after planting.

4. Rainbow Chard

Chard belongs to the chenopod food family, along with beets and spinach. It’s an excellent source of vitamins C, E, and A (in the form of beta-carotene) along with the minerals manganese and zinc. It’s a hearty plant that grows easily, and it makes a striking addition to your garden with its bright red stems.

Plus, chard degrades quickly during shipping, making it ideal to grow at home. Plant chard in early spring, and you’ll be able to harvest it all season long.

5. Bok Choy

Bok choy, which is also referred to as Chinese white cabbage, contains vitamins C and K, plus a higher concentration of beta-carotene and vitamin A than any other variety of cabbage. It also contains important nutrients such as calcium, magnesium, potassium, and manganese, all wrapped up in an extremely low-calorie package

Bok choy can be planted early spring through midsummer. Its leaves can be harvested when they’re about three inches tall, or you can wait until a head forms and harvest the whole plant at once.

6. Herbs

Fresh herbs can make your meals pop, but they’re expensive to purchase in the store. Fortunately, it takes very little space or skill to grow your own. You can even grow them on a windowsill. Some basic herbs to start with include basil, chives, cilantro, parsley, thyme, and dill.

7. Cherry Tomatoes

While regular tomatoes are relatively easy to grow, they can be sensitive to different temperatures. Cherry tomatoes are even easier, and you’ll be rewarded with pint after pint of the fruits that taste far superior to store-bought versions (plus they’ll be free of pesticides and fertilizers).

Cherry tomatoes like a sunny spot to grow, and you’ll need to tie them to a supportive stick or tomato cage as they grow.

8. Cucumbers

Cucumbers grow quickly and easily, and once you taste your homegrown version, you won’t want to go back to store-bought. These vines like to climb, so plant them near a trellis or fence, and put the seeds in only after the soil is warm.

9. Peas

Snap peas are another “vertical” grower, making them ideal when space is tight. Plant peas in early spring and plan to tie them to a small trellis for support when they start to get tall.

10. Carrots

Don’t let carrots intimidate you just because they grow below ground – they’re quite hearty and easy to grow for beginners. The seeds may take a few weeks to sprout and the carrots are usually ready to harvest in 46 to 65 days. As Matthew Benson, author of Growing Beautiful Food and farmer of Stonegate Farm in New York, told TIME:4

“‘We know less about what’s going on under our feet than we do what goes on up in the cosmos,’ says Benson. ‘It’s so mysterious, all of these interesting relationships between roots and rhizomes and microbes and all these cellular chatter that goes on in the dirt.’ Pulling veggies from the soil can be very satisfying for a first time farmer.”

11. Edible Flowers

Edible flowers like nasturtium add color to your garden and can add intense flavor to your meals. Plus, nasturtium is known to naturally repel pests like whiteflies, squash bugs, and striped pumpkin beetles. It takes about one to two weeks from planting for flowers to develop (simply snip the petals off for eating). These can even be grown indoors in pots.

How to Create Healthy Soil

The key to growing nutrient-dense food is to have soil that is abundant with microbial life and nutrients. Sadly, very few of us have access to this type of soil, but the good news is that it is relatively easy to create it. Paul Gautschi has been a personal inspiration to me in this area, and his garden is a testament to the fact that growing large amounts of healthy food can be very simple, and doesn’t require a lot of time.

The documentary Back to Eden was my first exposure to his work. I struggled for years seeking to unlock the puzzle of growing nutrient-dense food before I came across his recommendations—the simplicity and low cost of which really appealed to me. After studying his technique more carefully, I realized that using wood chips is probably the single best way to optimize soil microbiology with very little effort.

You can actually use virtually any organic material for mulch but wood chips seem to be one of the best, as they are concentrated sources of carbon that serve to feed the complex soil ecology. Typically, carbon is one of the nutrients that is far too low in the soil.

Additionally, by covering the soil around your plants and/or trees with mulch, you mimic what nature does naturally, and in so doing, you effortlessly maximize the health of the soil. Actually, the effortlessness comes after you do the hard work of moving the chips to where you need them to be. But once there, over time they work their magic and virtually eliminate the most concerning garden tasks, which is weeding, watering, and fertilizing.

Biochar is another great tool to help building your soil, the surface area of biochar is what gives it such great qualities when used in farming or gardening. The chips and leaves gradually break down and are digested and redigested by a wide variety of bacteria, fungi, and nematodes in the soil. Once the carbon can’t be digested anymore, it forms humates that last in the soil and provide a host of benefits that I will describe below.

Drastically Cut Down on Weeding and Watering

Other gardeners till the wood chips into the ground, which is by far your worst option. It’s actually important to avoid tilling the earth as it tends to destroy soil microbes, especially the complex and delicate mycorrhizal fungi. When you use wood chips as ground cover, tilling becomes completely unnecessary.

A few short months after putting down a deep layer of wood chips, you will end up with lush fertile soil beneath the chips that will happily support whatever you choose to grow. It is important to never plant in the actual chips, you need to move the chips back and plant in the soil and then cover the plant to below the first leaves.

One major reason why most people don’t want to garden is they abhor weeding. Wood chips will radically reduce your weeding, probably by over 90 percent, and the weeds that do grow are easily pulled out by their roots so it becomes relatively effortless to keep the area clean.

Many parts of the country are also challenged with droughts and may not get more than 10-20 inches of water a year. Wood chips are the ideal solution, as they will eliminate water evaporation from the soil. Better yet, at night they will grab moisture from the air and release it into the soil in the day when the soil needs it.

The Benefits of Gardening Go Far Beyond the Food

Gardening can provide you with a variety of fruits and vegetables to feed your family, but it also gets you outdoors in the fresh air and sunshine, helping your body produce much-needed vitamin D. It gets you moving, providing important exercise, and allows you to connect socially with other gardeners. It’s also good for your mental health.

A systematic review examined the impact of gardens and outdoor spaces on the mental and physical well-being of people with dementia. The research suggested that garden use, whether it be watering plants, walking through a garden, or sitting in one, lead to decreased levels of agitation or anxiety among the patients.5

Researchers in the Netherlands have also found that gardening is one of the most potent stress-relieving activities there is.6 In their trial, two groups of people were asked to complete a stressful task; one group was then instructed to garden for half an hour while the other group was asked to read indoors for the same length of time.

Afterward, the gardening group reported a greater improvement in mood. Tests also revealed they had lower levels of the stress hormone cortisol compared to those who tried to relax by quiet reading.

According to a survey by Gardeners’ World magazine, 80 percent of gardeners reported being “happy” and satisfied with their lives, compared to 67 percent of non-gardeners.7 Perhaps it’s no coincidence that gardeners are happier…

Mycobacterium vaccae is a type of bacteria commonly found in soil. Remarkably, this microbe has been found to “mirror the effect on neurons that drugs like Prozac provide.”8 It helps to stimulate serotonin production, helping to make you feel happier and more relaxed. No wonder so many people describe their garden as their “happy place.”

Bad Luck Causes Most Cancer, New Study Finds

Cancer cells in a culture from human connective tissue.

Humans want to believe we control our own destinies. If we exercise for 30 minutes every day, eat healthy, avoid cigarettes, alcohol, and drugs, meditate, and participate in the health trend du jour, it seems logical that we will live longer, be happier, and avoid diseases like cancer. Unfortunately, it seems fate is more chaotic than that. A new study published in Science suggests that most cancers are unavoidable. They’re caused more often by bad luck than anything else.

Mutation, which drives cancer, is actually totally normal. In fact, its the engine of evolution–if not for mutation, our genes wouldn’t make the random changes that once in a while end up giving us a new, important skill–like making enzymes that break down lactose, or resistance to disease. But often, those mutations get out of control. Cells divide and divide until they overpower the useful cells in our body and kill us. That’s what cancer is.

According to Bert Vogelstein and Cristian Tomasetti at the Johns Hopkins Kimmel Cancer Center, many of these cancers are unavoidable. They’re just part of nature.

“We all agree that 40 percent of cancers are preventable,” Vogelstein said at a press conference. “The question is, what about the other cancers that aren’t known to be preventable?”

Vogelstein explained that each time a cell’s DNA is copied, mistakes are made. Most of these mistakes are harmless, and as noted above, some of them can even be beneficial. “But occasionally they occur in a cancer driver gene. That’s bad luck,” Vogelstein says. Several of these bad-luck mistakes can add up to a cancerous cell.

Their study sets out to determine how often these mistakes are preventable–whether by not smoking or maintaining a healthy weight–how often they are genetic, and how often they occur by chance. The answer may surprise people who have spent decades believing they can control the development of cancer in their bodies. According to the paper, 66% of cancerous mutations are random, 29% are preventable, and only 5% are genetic.

The numbers vary depending on the type of cancer. Lung cancer is indeed usually caused by cigarette smoke, while childhood cancer is often random. The authors hope that these statistics will help some parents feel less responsible for their children’s disease.

An earlier paper by the authors on the same topic stirred up controversy in the scientific community. Some feel that publicizing this viewpoint will make people less likely to follow advice about cancer prevention. This new study is likely to be even more controversial.

Of course, cancer science is incredibly complicated. Mutations are not the only thing that matter in driving cancer. Factors like hormones can also play a role in determining who the disease hits hardest. “We’re not saying the only thing that determines the seriousness of the cancer, or its aggressiveness, or its likelihood to cause the patient’s death, are these mutations,” Vogelstein told NPR. “We’re simply saying that they are necessary to get the cancer.”

Source: Science via NPR

The Amount of Food Spiders Eat Each Year Will Haunt You for the Rest of Your Life

Spiders are already horrifying, with their eight beady little eyes and spindly legs and sticky webs. They also probably eat more meat than your mind can wrap your head around—more meat than humans eat, even.
 Spider meal specialist Martin Nyffeler of the University of Basel, Switzerland decided, hey, let’s try and estimate the total weight of all of the food spiders around the world eat per year. Some data crunching resulted in a number so bafflingly high you’ll either squirm or thank the spiders for keeping us safe from all the other bugs. Maybe both.

That number: The world’s estimated 25 million metric tons of spiders eat between 300 and 800 million metric tons of food per year, according to estimates published today in the very silly-sounding journal The Science of Nature. (That almost feels like calling something the Ferrari of Lamborghinis in academic journal speak). That food consists mainly of insects, little non-insect bugs called springtails, and even small vertebrates. The researchers make several assessments, using the amount of food individual spiders need to eat, the number of insects they catch in their webs, and the number of insects they kill on the hunt.

The 300 to 800 million metric ton figure is pretty close to the mass of meat and fish humans eat per year—around 400 metric tons, according to the paper. It’s also equal to the mass of humans: There are 7.4 billion people on earth, and the average human’s weight is around 130 pounds. Converted to metric tons, that’s a bit over 400 million.

 The idea to do this eye-opening calculation came from a book Nyffeler read 40 years ago, The World of Spiders by arachnologist William Bristowe in 1958, according to a prepared statement he passed along to Gizmodo. “In this book, Bristowe speculated that the weight of insects annually killed by the British spider population would exceed the combined weight of the British human population,” wrote Nyffeler. “This statement fascinated me very much. I decided that I would like to find out if Bristowe was correct with his speculation.”

You might think this means spiders are helping our crops by eating all of the pests, but that doesn’t seem to be the case. “Instead spiders appear to play a significant ecological role as predators of insects in forests and undisturbed grasslands,” Nyffeler wrote. Very generally speaking, spiders don’t seem to eat as many bugs in agricultural areas because these heavily managed systems don’t have as many or as good an assortment of prey.

Our apologies for that horrible image. But hey, at least they aren’t eating you. Yet.

Source:The Science of Nature