Parasitic infections occur when parasites grow, reproduce, or invade organ systems, making their hosts ill. Some natural health practitioners suggest that parasite infections can be treated with a cleanse comprised of herbs and supplements. The goal of a parasite cleanse is to treat a parasitic infection without over-the-counter (OTC) or prescription medications. However, very limited research supports these claims, and little research suggests that parasite cleanses are an effective treatment method.
What is a Parasite Cleanse?
Parasite cleanses are any diet or herbal supplement regimen meant to rid the body of parasitic infections. Parasites are organisms that infect other organisms and feed off their host’s nutrients. In humans, common types of intestinal parasites includes single-celled organisms like Giardia and various kinds of worms like tapeworms. Many manufacturing companies and wellness influencers who tout the use of parasite cleanses claim that most people have parasites in their bodies and don’t even know it. They encourage others to use these cleanses even if they haven’t been diagnosed with an infection by a doctor.
Understanding Parasitic Infections
A parasite is an organism that lives on or within the blood, tissues, or intestines of a host. External parasites, such as ticks, lice, or mites, are known as ectoparasites. In this case, though, we are talking about human intestinal parasites. These are divided into two categories: protozoa and helminths. Protozoa are one-celled organisms that are able to multiply within the host. Helminths are multi-celled organisms that fall into three main groups: tapeworms, roundworms, and thorny-headed worms. The most common method of transmission of intestinal parasites is eating or drinking something that has been contaminated with feces from an infected individual. Helminth infections can also be acquired from soil in which infected feces is present. Helminth eggs can attach to produce and can be ingested in contaminated water. During a certain part of their life cycle, hookworms can actively penetrate skin. Contact with contaminated soil can result in infection. Symptoms of parasite infection can include abdominal pain, bloating, gas, diarrhea, anal itching, unexplained weight loss, and exhaustion.
Natural Ingredients and Herbal Supplements
Very limited research exists on whether any natural ingredients may help treat parasite infections, but some people suggest the following herbal supplements may be beneficial:
- Anise
- Thyme
- Rosemary
- Cumin
- Marjoram
- Barberry
- Berberine
- Black walnut
- Clove oil
- Mint
- Goldenseal
- Grapefruit seed extract
- Propolis
- Oregon grape
- Wormwood
Many plant-derived products available in-store and online are also marketed to cleanse parasites from various body systems, including the intestines, liver, and other parts of the digestive tract. Some herbal detox programs last 2 weeks on and 2 weeks off, while others may last up to 1 month. However, no research supports the efficacy of any of these products and programs.
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Scientific Evidence on Natural Ingredients
Very limited research exists on the effectiveness of natural parasite cleanses. That said, some animal studies suggest that the following natural ingredients may have anti-parasitic effects:
- Thyme
- Rosemary
- Cumin
- Marjoram
- Garlic
- Ginger
- Tongkat ali
- Wormwood
- Berberine, which is found in barberry
- Propolis, which is made by bees
According to a 2024 review, some animal studies found that probiotic therapy may play a possible role in treating parasitic infections by increasing the healthy bacteria in your gut and promoting antibacterial activity. Similarly, a 2017 review found that vitamin A, zinc, and selenium may reduce the severity of parasitic infections. Supplementing with these minerals and vitamins might, therefore, form part of a parasite cleanse. Despite these results, however, all the researchers agree that more research in humans is necessary to determine whether any natural spices, herbs, and supplements have any benefits for treating parasites.
Dietary Recommendations
Healthcare professionals haven’t established a specific parasite cleanse diet. Preventing constipation is important because parasites are largely expelled from the body through stool. Some tips to help avoid constipation and possibly help treat parasites may include:
- Eating high fiber foods
- Eating a balanced diet of whole grains, lean proteins, fruits and vegetables, and low fat dairy products
- Limiting added sugars, refined grains, ultra-processed foods, alcohol, and high fat foods
- Eating garlic, ginger, and foods high in vitamin A
- Taking supplements, such as probiotics, vitamin A, zinc, and selenium
It’s also important to avoid eating raw or undercooked meat and seafood. If you have a parasitic infection, consider speaking with a healthcare professional about the best diet for you. They could recommend specific foods to eat and limit.
Cleansing diets or programs will often recommend a person eat a supportive diet while taking the product. This diet may include avoiding greasy, processed foods and eating natural, whole foods. Some parasite-cleansing diets ask the person to avoid specific types of foods, such as gluten, dairy, or pork. Diets may also include the use of anti-inflammatory herbs and spices, such as garlic, turmeric, and ginger.
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There is no evidence to suggest that following a specific diet will get rid of parasites from the body. However, many so-called “parasite cleanse diets” may make a person feel better simply by removing processed and greasy foods and introducing healthy probiotics and antioxidants. Although eating a varied and balanced diet, with plenty of fruits and vegetables, will benefit a person’s overall health, it is always best to consult a doctor before following a specific diet.
Risks and Side Effects
Limited research exists on the possible side effects of natural parasite cleanses and the associated herbs and supplements. For instance, some products for cleanses may contain dangerous ingredients or be marketed with false claims. Cleanses are also associated with several risks, such as:
- Diarrhea
- Malnutrition
- Kidney problems
- Dehydration
- Electrolyte imbalances
Expert Opinions and Clinical Perspectives
The notion of parasite cleanses isn’t new. There are no proven population-based, controlled studies to support this recommendation. Many people around the world, particularly in developing countries with inadequate sewer systems, do have intestinal parasites. According to research published in BioMed Research International, it’s estimated that 30 to 60 percent of these populations have parasites at some point in their lives.
However, this isn’t the case in the United States. Here in the United States, we're really fortunate to live in a state where there is well-serviced sanitation and sewer systems. So while it’s certainly possible to have a parasitic infection while living in the United States, it’s relatively rare.
How to Know if You Have a Parasite
Normally, parasite infections occur when eating or drinking contaminated food or water. For Americans, this may happen when traveling abroad to tropical or subtropical countries.
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Depending on the parasite, symptoms can include:
- Abdominal pain or cramping
- Nausea
- Vomiting
- Diarrhea
- Constipation
- Blood in your stool
- Fever
- Unexplained weight loss
Of course, these symptoms could be caused by any number of health issues, so it’s important not to assume you have a parasite or try to self-treat with a cleanse. If your digestive issues have been ongoing or if you have concerning symptoms like bleeding or unexplained weight loss, talk to your doctor.
If you experience symptoms of a parasite infection, speak with a doctor. They could perform several tests to check for parasites, such as stool tests, endoscopy, blood tests, and imaging tests like X-rays.
Medical Treatment Options
Some parasitic infections may go away on their own, but many require treatment. The specific type of therapy will depend on the parasite. Some infections can be treated with antibiotics, while others will need a class of drugs called anthelmintics. If left untreated, parasitic infections can have a number of complications, including anemia, weight loss, intestinal obstruction, and an increased risk of bladder and liver cancer. Some parasitic infections are very invasive and they can embed themselves into the lung, liver, or brain, which can turn fatal. That’s why it’s important to get a diagnosis and appropriate therapy if you have a parasitic infection.
Regulations and Supplement Safety
In addition to the potential complications associated with not getting the appropriate treatment if you do have a parasite, there are some other risks of parasite cleanses to consider. First, if the cleanse involves taking supplements, it’s important to know that these aren’t tightly regulated. The Food and Drug Administration does not have the authority to approve dietary supplements for safety and effectiveness before they’re sold. The concern with this is that you don't know how much you're taking and at what quantity and what unwanted side effects that might carry. Even benign or nonharmful things, when taken at exorbitant or unhealthy amounts, can become dangerous. What’s more, certain supplements may have interactions with prescription medications or other supplements you might be taking. It’s always recommended to speak to your doctor before starting any new supplements.
Deworming Naturally
Depending on the type of parasite infection you have, some infections may clear up on their own without treatment. Limited research suggests that natural ingredients alone can treat parasitic worms, but ingredients like thyme, rosemary, garlic, ginger, and probiotics may possibly help. It’s best to speak with a doctor, who will likely prescribe a medication to help treat the parasite infection.
Nutritional Immunology and Parasitic Infections
Nutritional immunology, immunometabolism, and identification of novel immunotherapeutic targets, are areas of active investigation in parasitology. There is a well-documented crosstalk among immune cells and cells in metabolically active tissues that is important for homeostasis. The numbers and function of these cells are altered by obesity leading to inflammation. A variety of helminths spend some part of their life cycle in the gastrointestinal tract and even entirely enteral nematode infections exert beneficial effects on glucose and lipid metabolism. The foundation of this review is the ability of enteric nematode infections to improve obesity-induced type 2 diabetes and the metabolic syndrome, which are significant health issues in developed areas. It considers the impact of nutrition and specific nutritional deficiencies, which are occur in both undeveloped and developed areas, on the host’s ability mount a protective immune response against parasitic nematodes. There are a number of proposed mechanisms by which parasitic nematodes can impact metabolism including effects gastrointestinal hormones, altering epithelial function, and changing the number and/or phenotype of immune cells in metabolic tissues. It is estimated that one third of the world’s population is infected with parasitic helminths with the greatest burden in underdeveloped nations particularly Nigeria and the Congo (1). Nutrients are cofactors and activators for the developing immune system (2) and malnutrition as well as bacterial co-infections are frequent in these developing areas and promote the chronicity of helminth infection. There is also increasing recognition that specific deficiencies in vitamins and/or minerals can contribute to the severity of parasitic infections in endemic areas. Alternately, well developed urban areas with the lowest worm burden have a much greater incidence of metabolic diseases including obesity-induced type 2 diabetes (T2D) and the metabolic syndrome. There is a well-documented crosstalk among immune cells and cells in metabolically active tissues that is important for homeostasis. Parasitic nematodes or their products can impact cellular metabolism by a number of mechanisms including direct effects on hematopoietic and non-hematopoietic cell function or indirect effects mediated by downstream activation of genes that regulate production of metabolically active factors. There are a variety of helminths, including parasitic nematodes, which spend a large portion of their life cycle in the gastrointestinal (GI) tract. Their presence in the lumen initiates, extends, or amplifies signals that are critical to host defense against parasites. For most of human history, malnutrition was common, and the effect of malnutrition on immunity, especially cellular immunity, has been studied extensively (4). A systemic review of the effects of malnutrition in children reported reduced gut barrier function, atrophied lymphatic tissue, and polarized cytokine production toward a Th2 response (2). The skewing of cytokine production toward a Th2 response; however, does not necessarily translate into improved resistance to nematode infections. Mice fed diets with reduced protein content showed delayed expulsion of primary Nippostrongylus brasiliensis (N. brasiliensis), Trichinella spiralis (T. spiralis) and Trichuris muris (T. muris) infections (5) and the Th2 response to a secondary Heligmosomoides polygyrus bakeri (H. polygyrus bakeri) infection was impaired resulting in increased worm burden (6). Similarly, mice infected with H. polygyrus bakeri and fed a diet with adequate protein and nutrient levels, but reduced caloric content, showed impaired lymphocyte proliferation, reduced Th2 cytokine production with lower levels of IgE, parasite-specific IgG1, and eosinophils, resulting in higher worm burdens and fecundity (7). In a recent study using multiple small (trickle) infections with H. polygyrus bakeri to mimic natural infections, the tolerance to infection, as measured by intestinal barrier function, was decreased by protein malnutrition (8). In the twentieth and twenty-first centuries, consumption of “Western diets” has led to excessive caloric intake, increased consumption of highly refined foods, and decreased consumption of fruits and vegetables that may lead to deficiencies in at-risk populations including the elderly, the economically disadvantaged, or those with diseases that contribute to impaired absorption including Crohn’s disease, ulcerative colitis, and parasitic infections (9, 10). In particular, both gastrointestinal diseases and parasitic infections have been shown to impair micronutrient absorption.
Vitamin A
The role of vitamin A in immunity is highly pleiotropic. The effects are dose-, receptor form-, cell type-, and environmentally-dependent (reviewed in (11)). Dietary vitamin A or retinol is converted to retinaldehyde by ubiquitous alcohol dehydrogenases and then irreversibly acted on by cell-specific retinaldehyde dehydrogenases to generate its active metabolite, retinoic acid (RA), which binds to the RAR and RXR nuclear receptor families and function as transcription factors (11). RA can be produced locally by migratory CD103+ dendritic cells and macrophages in the lamina propria, and by stromal cells in the mesenteric lymph nodes and bone marrow (12, 13). In addition, RA is elaborated by intestinal epithelial cells that, in turn, promote gut-homing of IgA secreting B-cells (14), CD4+-, and CD8+ T cells (15, 16), a process that is impaired in vitamin A deficient mice (15, 17). RA can act as a suppressor or activator of an inflammatory response depending on the circumstances. RA provides a critical signal for iTreg cell differentiation and iTreg cells can inhibit Th1- and Th17-type inflammatory responses (19-21). iTreg cells are decreased in vitamin A deficient mice leading to impaired oral tolerance (22). Differentiation of CD4+ T-cells is dependent on both vitamin A and RARα. Production of IFN-γ and IL-17A is decreased in T-cells lacking RA signaling and Th17 cells are severally reduced in vitamin A deficient mice (23). RA is important for maintenance of polarized Th1 cells and preventing conversion of Th1 cells to dual IFN-γ/IL-17-expressing Th17 cells (24). In contrast, RAR signals favor Th2 differentiation in naïve T-cells (25), is mediated via cytokine production by APC (25), and can impact resistance to parasitic infections which are classic inducers of Th2 immunity. This is important as the WHO showed that regions where soil-transmitted helminthiasis is most prevalent, Central America, especially Mexico, Central Africa, and Southeast Asia, are also areas of endemic vitamin A deficiency. Both low and high doses of RA increased localized Th1, Th2, Treg, and inflammatory responses in the liver and lung of Ascaris suum-infected pigs as well as increased BAL eosinophilia that may be related to enhanced induction of eosinophil chemokine activity by alveolar macrophages (26). The increase in type 2 innate lymphoid cells (ILC2) cells in vitamin A deficient mice was associated with increased resistance to a T. muris infection (23) that was dependent on fatty acid oxidation (27). This finding extends earlier work where egg excretion decreased more rapidly in Trichuris suis-infected, vitamin A deficient pigs than in vitamin A sufficient pigs (28), but contrasts with the increased parasite burden in Litomosoides carini-infected, vitamin A deficient cotton rats (29). Although worm expulsion was only slightly reduced in T. spiralis infected vitamin A deficient mice, differences in the immune response between sufficient and deficient mice were observed including higher IFN-γ and lower IL-4 production in MLN of infected deficient mice (30). Mice with a chronic infection of T. muris have reduced enzyme activity of and cell percentage staining for retinal dehydrogenase in lamina propria-derived dendritic cells and macrophages that did not rebound until the infection was cleared, indicating that chronicity may be related to decreased local RA levels (31) and impaired immune responses. The cause of this reduction was not identified, but may be a regulatory mechanism used by the parasite, or may result from reduced vitamin A absorption (32).
Selenium
Selenium (Se), via its incorporation into selenocysteine-containing proteins (Sels), has substantial effects on immune function. There are 25 Sels identified in humans and 24 in mice with only partially characterized function. Selenium is important for both humoral and cell-mediated responses including cytotoxic T-lymphocytes and natural killer cells (33), chemokine and cytokine responses to viral infections (34, 35), respiratory burst (36), and for protection against LPS-induced oxidative stress (37). Specific Sels have been implicated in immune function. Both glutathione peroxidase 1 (GPx1) and glutathione peroxidase 2 (GPx2) are important for controlling Th2-dependent allergen-induced airway inflammation (43) with knockout of GPx1 shifting the Th cell bias toward Th1 and suppressing development of Th17 cells (44). Thioredoxin reductase maintains thioredoxin in its reduced state and thioredoxin is important for immune function and cell survival (45). Selenoprotein K KO mice exhibit aberrant calcium signaling in immune cells and an impaired immune response (46). Selenoprotein S is linked to regulation of inflammation (47). Se status affects the immune response to parasitic infections. Selenium deficiency resulted in delayed expulsion of H. polygyrus bakeri (51, 52) due at least, in part, to decreased Th2 responses and production of Relm-β, a goblet cell protein critical for worm expulsion (53). Similarly, Se deficiency impaired clearance and reduced the Th2 response to N. brasiliensis infection in mice, an effect also observed in mice with conditional knockout of selenoprotein expression in macrophages (54). This effect of N. brasiliensis infection was attributed to the reduction in the transcription factor proliferator-activated receptor-γ (PPAR-γ)-mediated switch from a classically activated (M1) to an alternatively activated (M2) macrophage phenotype (55).
Zinc
Zinc deficiency leads to atrophy of the thymus, a reduction in leukocytes, as well as in antibody-mediated, cell-mediated, and delayed-type hypersensitivity responses (58). In addition, NK cell activity is decreased in neutrophils, and macrophages have reduced levels of phagocytosis and respiratory burst in zinc deficiency (59). Production of the Th1 cytokines IL-2 and IFN-γ is attenuated by zinc deficiency resulting in a shift toward a Th2 response (60). Basal levels of pro-inflammatory cytokines are elevated in zinc deficiency, but production is ablated upon stimulation (61). Decreased cytokine production may result from decreased NF-κB activation in zinc deficiency (62, 63). Both immature and mature B-cells are reduced by zinc deficiency (64) as is antibody production (65). Zinc was found to increase Treg cell numbers in allergen-stimulated cells from atopic subjects and in mice with experimental autoimmune encephalitis (66, 67). Significantly, moderate zinc deficiency (3 mg/kg diet) in rats delayed expulsion and increased worm burden of T. spiralis, egg excretion, but not worm burden of N. brasiliensis, and delayed clearance of Strongyloides ratti (68). Moderate and severe (0.75 mg/kg), but not marginal (5 mg/kg) zinc deficiency, impaired the Th2 response to H. polygyrus bakeri and prolonged worm survival in primary H. polygrus bakeri-infected mice while in a challenge infection, only severely deficient mice had an impaired Th2 response and increased worm burdens (69). These data indicate that zinc deficiency impairs the Th2 response to parasitic infections and that zinc is important for Th2 immunity to parasitic infections.
Malnutrition and Obesity
The impact of malnutrition and micronutrient deficiencies was focused for many years on developing nations. In areas of endemic infection, parasitic helminths that have evolved strategies that favor chronic infection are common (1) and the adverse effects of nutritional deficiencies to host defense further compound chronicity. Despite the epidemic of obesity and the metabolic syndrome in the United States and across the world, obese patients are often malnourished and exhibit similar deficiencies in micronutrients (70). The World Health Organization (WHO) estimates that 39% of adults aged 18 years and over were overweight in 2014, and 13% were obese in the world. There is little information on the impact of obesity on type 2 immune responses. Obesity prone mouse strains however, are more susceptible, while lean mouse strains were more resistant, to parasitic nematode infection (71). Obesity induces a wide variety of inflammatory and stress responses in metabolic tissues and higher concentrations of circulating inflammatory markers. This results in chronic, low grade inflammation termed “metaflammation” (72) which is central to insulin resistance and disruption of insulin receptor signaling (73), and requires the participation of both immune and non-immune cells. This has fostered the emerging field of immunometabolism that is focused on investigating the pro-inflammatory cytokines and mediators of obesity, the metabolic syndrome, and T2D (74). The surface epithelial cells that line the GI tract form the first line of defense in the gut and include the absorptive enterocytes, the mucus-producing goblet cells, and the hormone-secreting enteroendocrine cells (EEC). Along with immune cells, epithelial cells transduce specific pathogen-derived signals into effector functions; however, the mechanisms by which a wide variety of helminths induce a Th2 response remain to be elucidated. A confounding issue is that helminths elaborate antigens and excrete and secrete (E/S) a variety of products that may be involved in the initiation and maintenance of the type 2 immune response. How the cells respond to E/S products is also unclear, but highly implicated are pattern recognition receptors (PRR) and membrane-associated toll like receptors (TLR) that recognize conserved features of pathogens. Worm-derived proteases may play a role in transducing the density and location of nematodes in the intestinal lumen (76). PAR-2 expression is ubiquitous along the GI tract and is expressed by epithelial cells, enteric nerves, and smooth muscle cells as well as by a variety of immune cells, including mast cells, macrophages, and T cells (77). Activation of PAR-2 on enterocytes increases epithelial permeability and fluid secretion from enterocytes and also enhances the nerve sensitivity of visceral afferent nerves (76), effects that are important for worm expulsion (78-81). Of interest is that in functional GI disorders, such as IBS, these effects are amplified and/or unresolved (82, 83). The reduced barrier function …