Medicinal Herbs and ADHD

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Resolving Pain & Inflammation and Healing Connective Tissues

Part of the Clinical Practicum series on WholisticMatters designed to bring you clinical information for your practice.

 Herbal Approaches

Abstract

This paper will address how to address pain and inflammation with herbal medicine within a clinical setting from a primarily systems vs. symptoms-based approach. Major mechanisms of action of key herbs will be explored while providing the clinician with a deeper knowledge of a plant’s tissue specify & secondary actions, and thus ability to better individualize treatment protocols, taking a more holistic approach to the management of pain, inflammation and connective tissue healing. Herbal approaches to the resolution of pain & inflammation through the modulation (vs. inhibition) of inflammatory pathways demonstrates a supportive (as opposed to suppressive) therapeutic intervention where the resolution of inflammation can be achieved whilst connective tissue function is both nourished and restored.

Clinical Challenges in Managing Pain & Inflammation

Pain is a complex, initially protective and adaptive response manifesting as a sensory, emotional, and cognitive phenomenon that can frequently out-live its usefulness and impede the body’s ability to function. It is universal to the human experience, and though it can vary greatly in subjective intensity and duration it is inextricable from the inflammatory process as all pain will involve an inflammatory component.1 Chronic inflammation results in pain and destruction of bone and cartilage that can lead to severe disability and in which systemic changes occur that can even result in the shortening of life.1 There are many different types of pain (see Table 1), and such pain pathways involve intricate connections between neurological networks, pain-sensing systems and other neuroendocrine networks.3 According to the National Institute of Health, pain is the leading cause of disability and affects more Americans than diabetes, heart disease, and cancer combined.4 According to the American Academy of Pain Management the most common types include arthritis, lower back, bone/joint pain, headaches, muscle pain and fibromyalgia.

Most conventional approaches to these conditions focus solely on the symptomatic reduction of pain and/or inflammation as opposed to addressing the underlying causes, contributing factors, or systems imbalances contributing to the patient’s dis-ease. Although alleviation of pain through the use of conventional analgesics & anti-inflammatories can be useful in some cases, our deepening understanding of the processes involved in the resolution of inflammation reveals that targeting singular physiological pathways (i.e. inhibition of pain pathways) is not always in the best interest of the patient, and can in fact in some cases impede the healing process, leading to chronic inflammation while carrying concerns with regards to addiction, dependence, as well as other serious and/or uncomfortable side effects. Moreover, taking this type of symptomatic approach ignores the many potential contributing mechanisms to pain & inflammation (see Table 2).

The transition from acute to chronic pain occurs in discrete pathophysiological and histopathological steps. Under normal conditions, painful stimuli diminish as tissue healing progresses, however persistent or intense pain activates secondary mechanisms that can diminish normal functioning and lead to chronic pain. This transformation of acute to chronic pain include processes involving prostaglandins, endocannabinoids, ion-specific channels to name a few.5 Chronic pain is more than a symptom, but an illness unto itself with its own set of comorbidities that has been increasing in prevalence and is considered to be the most underestimated health care problem impacting quality of life.6

Supporting the Resolution of Inflammation  

Inflammation is a healthy, normal defensive response to injury or irritation involving a complex cascade of immune response signaling and cytokines which are a necessary stage of resolution and wound healing. However when the resolution process is uncontrolled, chronic inflammation can act as the primary cause of a vast continuum of disorders with a variety of presentations, including chronic disease and even cancer.7,8 Additionally, inflammatory responses in the peripheral and central nervous systems play key roles in the development and persistence of many pathological pain states, as messenger molecules released from inflamed areas can lead to the inappropriate activation of a pain response. Our goal therefore should be to support and improve the control of these complex biological processes whenever possible, and this may be considered difficult if not impossible to accomplish through the use of single targeted therapeutic mechanisms.

Inflammation involves the sequential activation of signaling pathways leading to the production of both pro- and anti-inflammatory mediators. The pro-inflammatory signaling pathways and cellular mechanisms that initiate the inflammatory response have become well characterized, however those mediators and mechanisms that switch off inflammation are only more recently coming to light. Current data indicate that the resolution of inflammation is an active process controlled by endogenous mediators that suppress pro-inflammatory gene expression and cell trafficking, as well as induce inflammatory-cell apoptosis and phagocytosis, which are crucial determinants of successful resolution.9 For example, it has been demonstrated that the transcription factor NF-κB, whose activation was primarily thought to have a central role in the induction of pro-inflammatory gene expression, is associated with the expression of anti-inflammatory genes and the induction of apoptosis, and inhibition of NF-κB during the resolution of inflammation protracts the inflammatory response and prevents apoptosis, suggesting that NF-κB actually has an anti-inflammatory role in the regulation of inflammatory resolution, thus its complete inhibition may in fact be detrimental in vivo.10

Table 1: Types of Pain
  • Mechanical damage/trauma (e.g. acute/nociceptive)
  • Joint (capsule stretch)
  • Ligaments (sprain, tear)
  • Muscle (strain, tear, spasm)
  • Tendon (strain, tear)
  • Radicular (impingement)
  • Acute vs. Chronic Inflammatory (”itis” vs. degeneration & Repetitive trauma/injury “osis”)
  • Systemic disease process (e.g. auto-immune, metabolic)
  • Vascular (claudication)

 

Table 2: Potential Contributing Mechanisms to Pain & Inflammation
  • Autoimmunity
  • Food Allergy & Sensitivity
  • Poor Gut health (chronic infections, alterations in microbiome)
  • Hormonal imbalance
  • Neuroendocrine disruption
  • Poor Diet and Hydration (Nutrient depletion)
  • Posture/Ergonomics
  • Stress/Depression/Anxiety
  • Sleep Disturbance
  • Lifestyle Factors
  • Socioeconomic Factors
  • Social Relationships & Support
  • Xenobiotic burden

 

Resolving Pain & Inflammation with Herbal Medicine

As we are learning, the resolution phase of inflammation is just as actively orchestrated as its induction and inhibition.11 Thus the treatment of pain and inflammation should not be restricted to the use of inhibitors of the acute cascade, but broadened to take account of the enormous therapeutic potential of inducers and/or modulators of the resolution phase of inflammation. This recent emphasis toward resolution is crucial towards our understanding of how immune-mediated inflammatory responses are actually terminated. Inflammatory responses, like all biological cascades, are shaped by a delicate balance between positive and negative feedback loops, and resolution involves reprogramming of cellular functions while simultaneously preparing tissue for regeneration after the cause of inflammation is removed.12 This is where the use of herbal medicine can be incredibly helpful, acting at multiple phases of healing and within various pro-resolution pathways as modulators, not suppressors, of the pro-resolving inflammatory process.

Many herbal medicines have the ability to act as mediators or modulators of inflammation while simultaneously reducing pain and aiding in tissue repair and regeneration. These herbs are often referred to collectively as Anti-rheumatics, which provides an umbrella term for many herbs that used traditionally to treat pain and inflammation of the muscles & joints. Even when administered at the onset of an acute inflammatory response they will allow the initiation phase to occur while often aiding in both the removal of tissue waste products and providing nourishment in the way of key macro/micro & phytonutrients. Relative to conventional drugs the majority of herbs generally carry a low risk of adverse effects, and can often be safely combined with existing pain treatments, and when combined together will often demonstrate synergetic effects on multiple pathways involved in the the propagation of pain & inflammatory signaling, as well as systems and tissue specific wound-healing (vulnerary) effects.

Herbal medicines will vary in regards to the quality and availability of clinical evidence, and certain plants will have much more known regarding their particular phytonutrient profile and mechanism of action. For example, “curcumin and inflammation” yields over 100,000 scholarly articles, while “California poppy & pain” yields a small fraction of that amount. When less is known regarding a particular herbal medicine the importance of drawing on traditional and historical uses of plants is encouraged, especially in relation to providing ideal dosing strategies and identifying obvious safety and/or toxicity concern. There are several plant constituents however where much more is known regarding their effects on pain & inflammation, for example the alkaloids found within the Papaveraceae family which act on our endogenous opioid system have been recognized as some of our most potent inhibitors of pain (both mental & emotional) for decades, endogenous cannabinoids in the cerebral cortex which also modulate pain sensation and responses, and the salicylates which appear to work primarily by interfering with production of prostaglandin synthesis & bradykinin during tissue damage and inflammation.13-15 As clinicians it can be helpful to look to herbs that operate within these pathways. Table 4 provides an overview of some potential target mechanisms when addressing pain and inflammation, while table 5 provides an overview of some of the most commonly recognized mechanisms of action, active constituents and herbal examples.

Table 3: Comparative Knowledge of Herbal Medicines
  • Traditional & historical uses
  • Tissue & organ system Affinity
  • Known secondary metabolite (constituent) profile, activity & bioavailability
  • Quality & availability of clinical evidence
  • Ideal method of herbal pharmacy, route of administration & dosing strategy
  • Adverse effects, toxicity concerns and/or drug interactions

 

Table 4: Target Mechanisms for Management of Pain & Inflammation
  • COX/LOX – Cytokines (bradykinin)
  • Opioid receptor system
  • Endocannabinoid system
  • Inhibitory Neurotransmitter Agonists (i.e. GABA, serotonin)
  • Endocrine – HPA axis (Cortisol agonist)
  • Immune (T1/T2 Modulation, histamine)
  • Excitatory Neurotransmitter Antagonist (i.e. Glutamate)
  • Topical Applications (i.e. substance P)

 

Table 5: Plant Mechanisms in Management of Pain & Inflammation16
Mechanism Constituent(s) Herbal Examples
Opioid Isoquinoline Alkaloids Corydalis spp. (Golden Smoke/Yanhusuo)

Eschscholzia californica (California poppy)

Prostaglandin Salicylates

Curcumin

Resin

Salix alba (Willow bark)

Tanacetum parthenium (Feverfew)

Curcuma longa (Turmeric)

Boswellia serrata (Frankincense)

Commiphora molmol (Myrrh)

Neurokinins (Substance P) Capsaicin Capscium spp. (Cayenne)
Cannabinoid Phytocannabinoids Cannabis spp. (Cannabis)
Ion Channels Resin (Kava lactones) Piper methysticum (Kava Kava)
Endocrine (HPA axis) Steroidal & Triterpenoid Saponins Withania somnifera (Ashwagandha)

Glycyrrhiza glabra (Licorice)

 

First Line: Herbal Anti-inflammatories (Inflammatory Modulators) & Analgesics

It is increasingly inaccurate to refer to herbs as anti-inflammatories at all, as they are in fact modulators of such physiological processes in a way that suits normal balance between inflammatory & anti-inflammatory mediators by maintaining a balance between cytokines and acting as antioxidants, immunomodulators, or any form of action that helps to inflammation process and normalize the immune response.17 Nonetheless, what are known as anti-inflammatory botanicals will also often have direct analgesic properties and might be considered in patients with inflammation-related pain. A number of botanical medicines have proven effective for relieving different forms of pain though a variety of physiologic mechanisms (see table 5) of which some have been well delineated and others are less well understood. Analgesic effects of herbs are typically slower acting than conventional ones but longer lasting, and will exert anti-inflammatory effects in a “concentration-dependent” or “dose-dependent” manner.18 It is also worth noting that many of these herbs are known to exert such effects when applied either topically or taken internally.

Table 6: First Line Herbal Anti-inflammatories & Analgesics
Herbal Example Key Clinical Indications Safety Concerns/Contraindications
Salix alba (Willow bark)
  • Acute & chronic pain specific to the musculoskeletal system (e.g. Arthritis, & low back pain).19-22
  • Systemic connective tissue conditions with inflammatory changes, neuralgia, and headache.
  • Theoretical additive effect with anti-platelet medications, salicylate-containing substances, NSAIDs, methotrexate, spironolactone, phenytoin, and valproate medications.
  • Use caution during lactation and in children under 15 (theoretical Reye’s syndrome).
Boswellia serrata (Frankincense)
  • Acute & chronic inflammation especially of the gastrointestinal tract, (e.g. ulcerative colitis, Crohn’s disease).23-27
  • Osteoarthritis & rheumatoid arthritis.28-29
  • Analgesic in acute MSK trauma (in combination with Turmeric)30
  • May cause stomach upset.
Commiphora molmol (Myrrh)
  • Chronic inflammation especially towards mucus membranes of the gastrointestinal tract.31
  • Analgesic & anti-inflammatory, in various pain pathologies potentially including headache, infection, joint pain, muscle aches, low back pain, and menstrual cramps in women.32,33
  • CI in pregnancy, excessive uterine bleeding and with long-term use (>few weeks), and in active inflammatory conditions according to TCM.
Curcuma longa (Turmeric)
  • Acute or chronic, local or systemic inflammatory conditions such as arthritis tendonitis, bursitis, bruises, sprains & pain and inflamed joints.34,35
  • In inflammatory gastrointestinal conditions (e.g. Crohn’s disease & ulcerative colitis).36
  • Used as a conjunctive therapy alongside conventional analgesics in several pain disorders (e.g. migraine).37-39
  • Use caution with biliary obstruction, gallstones, acute stomach ulcers, women wishing to conceive and in anemia.
  • May effect activity of certain chemotherapeutic drugs.
  • May have additive effects with NSAIDs & anticoagulants (theoretical), and possible antagonistic effects with immunosuppressants & beta-blockers at high doses.
Zingiber officinalis (Ginger)
  • Anti-inflammatory in rheumatic complaints (e.g. osteoarthritis, rheumatoid arthritis & gout) and analgesic in muscle spasm.40-44
  • Traditionally used as a circulatory stimulant to improve circulation to the limbs.
  • Potentially additive effects with antiplatelet medications. Theoretical interactions with anti-arrhythmics, anti-diabetic agents, and anti-hypertensives.
  • Use caution in those with sensitive stomachs as will not always tolerate, and with acute gastric with ulcers, GERD, gallstones, and bleeding disorders.

 

Addressing Contributing Causes:

Stress, Sleep & Mood Disorders

Studies on pain–depression comorbidity have shown that: (a) pain is as strongly associated with anxiety and depressive disorders, and (b) certain psychological symptoms (low energy, disturbed sleep, worry) are prominent among pain patients.45 It is also a common clinical experience that anxiety about pain can exacerbate the pain sensation. Chronically painful conditions are frequently associated with sleep disturbances, and it is becoming increasingly recognized that disturbances of sleep can in fact cause or modulate both acute and chronic pain.46 Interestingly, most of the herbal medicines used for improving sleep, stress and mood disorders (e.g. depression & anxiety) also have analgesic, antispasmodic, and anti-inflammatory activity. The mechanism of action of some of these herbs has yet to be fully elucidated, so most of our information is based on centuries of clinical experience. For safety, heavy machinery should not be operated while taking herbs in this category that have sedative effects, and clinicians should be aware that combining these herbs alongside other sedatives will likely have additive effects.

Table 7: Nervine Relaxants/Sedatives & Antispasmodics
Botanical Key Clinical Indications Safety Concerns/Contraindications
Corydalis spp. (Corydalis)
  • Sedative & antispasmodic (in combination with California Poppy and other herbs).47,48
  • Potential to increase pain tolerance, and treat opiate addiction.49-51
  • Traditionally used in dysmenorrhea and abdominal pain as an antispasmodic.
  • Avoid in pregnancy & lactation, children and patients with neurological disease (depression, psychosis, liver or kidney disease)
  • May have additive effects with anticoagulant and analgesic medications.
Eschscholzia californica  

(California Poppy)

  • Anxiolytic with normalizing effect on associated physical and psychological symptoms such as pain, neuralgia, migraine, stress, and nervous bowel.52-54
  • Traditionally used as a sedative and regulate sleep patterns in insomnia.
  • May have additive effects with analgesic medications and potentiate MAOIs.
  • Use caution in children, neurological disease, depression, psychosis, liver and kidney disease.
Piscidia piscipula

(Jamaican Dogwood)

  • Antispasmodic & analgesic traditionally used for pain of the uterus and skeletal muscle, especially indicated in insomnia, dysmenorrhea with associated nervous and/or musculoskeletal tension (e.g. migraine headaches and neuralgias).
  • High doses may cause bradycardia, hypotension, nausea, vomiting, numbness, tremor, sweating, headache, and paralysis.
  • Avoid in pregnancy, lactation, children and the elderly.
  • Use caution in CVD and cardiac insufficiency.
Passiflora incarnata

(Passionflower)

  • Sedative, antispasmodic, analgesic and anxiolytic, used for soothing nervous tension, restlessness, muscle spasm, and in mild cases of insomnia.55-59
  • Potential to aid in symptoms of opiate withdrawal.60
  • Possible mild nerve and muscle irritation with long-term use.
  • Potential additive effects with sleep aids, barbiturates and other CNS depressants.
Piper methysticum 

(Kava Kava)

  • Anxiolytic (especially in perimenopausal women & antidepressant.62-66
  • Analgesic and antispasmodic (reduce muscle tension).67-69
  • May assist in withdrawal from benzodiazepine drugs.70
  • Traditionally used as a topical for rheumatism, joint pain, neuralgias, chronic pain and restless leg syndrome.
  • Acute toxicity may cause CNS and motor disturbances.
  • Avoid when operating machinery, or when sedation could pose a danger, long-term, or excessive use.
  • Avoid in pre-existing liver damage or disease, when patients are taking drugs known to cause liver damage, or with history of excessive alcohol consumption.
  • May potentiate effects of CNS depressants (e.g. alcohol, barbiturates, benzodiazepines) and anti-platelet medications.
  • Possible dopamine antagonist effects when combined with L-dopa and other Parkinson’s disease treatments and other anti-psychotics.
Hypericum perforatum

(St. John’s Wort)

  • Analgesic and anti-inflammatory (topically and internally) particularly indicated for anxiety, mild to moderate depression, neuralgia (e.g. trigeminal, herpetic & sciatica) and gastrointestinal symptoms such as IBS.71-80
  • Possible side effects include digestive upset, allergic skin reactions, sleep disturbance, dizziness, bradycardia, heart palpitations, restlessness, and photosensitivity can occur in susceptible individuals with prolonged exposure ultraviolet light.
  • Use caution in history of mania, bleeding disorder, liver disease, seizure and disorder.
  • Avoid in pregnancy or lactation.
  • Avoid concomitant use with selective serotonin reuptake inhibitors due to possible potentiation effects which may result in serotonin syndrome. However, if clinically appropriate, may be safely combined under professional supervision. A low dose should be recommended and patient should be monitored for symptoms of serotonin syndrome (e.g. agitation, hypertension, delirium, sweating).
  • Speeds up the elimination of many drugs and may reduce activity/serum levels due to induction of CYP3A4 expression.
Viburnum opulus

(Cramp bark)

  • Antispasmodic and hypotensive traditionally used to relieve cramps and spasm of both skeletal and smooth muscle with tissue specificity to the uterus and blood vessels, however, muscle spasms, pain, and cramping in any area including back & leg pain, arthritis, and polymyalgia can benefit from its use.81,82
  • Regarded as a uterine tonic, to treat dysmenorrhea, and irregular uterine contractions, and has possible role in endometriosis.83
  • Nausea, vomiting and gastric upset may occur with large doses.
  • Use with caution during lactation
  • Theoretical additive effect with anti-platelet medications, salicylate-containing substances, NSAIDs, methotrexate, spironolactone, phenytoin, and valproate medications.
  • Use caution during lactation and in children under 15 (theoretical Reye’s syndrome).

 

HPA Axis Dysregulation

Adrenal hormones (i.e. norepinephrine (NE) & cortisol) are also integrally involved in the resolution of inflammation. The stress hormones produced by the HPA axis have a direct effect on the phases of inflammation and create downstream metabolic effects including insulin and cortisol resistance. Resolution of inflammation can only take place when NE is equal to the level of cortisol (plus insulin), and the stop signal for inflammation requires a low level of NE along with normalized cortisol sensitivity.84 Adaptogenic herbs can work on both by aiding in the resolution of the inflammatory process by modulating cortisol activity via the HPA access, as well as key mediators of inflammation. Sustained elevated cortisol levels can inhibit innate immunity & potentially lead to glucocorticoid receptor resistance, which disrupts the body’s ability to naturally resolve inflammation.85 It’s important to note that adaptogens do not inhibit the stress response, but improves stress response (often via hormetic effects), normalizing stress-induced elevated levels of cortisol and other extra/intracellular mediators of stress response (e.g. elevated NO, SAPK via upregulated expression of NPY and heat shock proteins).86

Table 8: Adaptogens  
Botanical Key Clinical Indications Safety Concerns/Contraindications
Withania somnifera

(Ashwagandha)

  • Anti-inflammatory with potential role in many chronic diseases (e.g. arthritis, autoimmune, neurodegenerative & neurobehavioral).87-90
  • Traditionally used to restore health to the nervous system in cases of stress & anxiety, nervous exhaustion, fatigue, loss of memory & muscular energy, convalescence, insomnia, and augment resistance of the body against disease.91-93
May potentiate the effects of CNS depressants and cause drowsiness and reduced coordination.

Avoid in patients with known allergy to Nightshades (Solanaceae family).

May cause digestive discomfort.

Glycyrrhiza glabra (Licorice)
  • Anti-inflammatory which alleviates pain in rheumatism (e.g. muscle spasm & and joint inflammation both internally and topically).
  • Inhibits the metabolism of corticosteroids and can support the adrenal cortex during chronic stress and be a valuable component of treatment for recuperation. May aid in the withdrawal of steroidal anti-inflammatory drugs and/or extend their pharmacological effects.94-97
  • Traditional used for treatment of peptic ulcers and to soothe gastrointestinal inflammation such as in GERD, gastritis, and IBD.98
  • Use with caution in hypertension, cardiovascular disorders, edema associated with heart failure, liver problems, kidney insufficiency, hypokalemia, hyperparathyroidism, male infertility or erectile dysfunction.
  • Avoid in pregnancy, lactation, and when on dialysis.
  • May decrease effectiveness of most anti-hypertensive medications and estrogen-based oral contraceptives, immunosuppressives, midazolam, & omeprazole.
  • May potentiate the action or increase levels of corticosteroids
  • May result in excessive potassium loss when combined with potassium-depleting drugs and potentiate the toxicity of cilostazol & digoxin.
Panax ginseng (Asian ginseng)
  • Used to increase resistance to stress, acting mainly on the hypothalamus and having a sparing action on the adrenal cortex. During prolonged stress will have a glucocorticoid-sparing effect while at the same time adrenal capacity is increased.99
  • Can help reduce fatigue and may have benefit in fibromyalgia and chronic fatigue syndrome100-102
  • Can improve resistance to infection and assist recovery from infection, disease or surgery.103,104
  • High doses may cause hypertension with nervousness, palpitations, chest pain, insomnia, headache, nosebleeds, and digestive upset, and may cause side effects related to an estrogen-like activity in women.
  • Avoid in history of arrhythmia, acute asthma, hypertension, acute infections, and ADHD. Use caution with acute infection and in hyper tense people and in children.
  • Avoid concurrent use with stimulants such as caffeine and amphetamines due to additive effects.
  • May decrease effectiveness of antihypertensive medications.
  • May potentiate effects of antiplatelets, hypoglycemics and sildenafil.
  • Theoretical interaction with anti-psychotics, MAOIs, sedatives, immunosuppressants, and other hormone therapies.

 

Healing & Supporting Tissue Damage

Resolution of inflammation must involve tissue repair & regeneration.105 Once pain and inflammation have been adequately controlled herbs can be employed to help speed wound healing, collagen formation, angiogenesis, and increase antioxidant levels within the wound especially in early stages of tissue repair. Promoting the repair of damaged connective tissue shortens the wound healing process and in some cases may suppress the formation of scar tissue.

The herbs which are used to this end are often highly nutritional and can support circulation & improve the health and integrity of the microvasculature through phytonutrients such as bioflavonoids, saponins and allantoin. In this way many act as “alteratives” (aka. tissue detoxifiers) that can improve the removal of metabolic waste products through the lymphatic systemic and this reduce tissue swelling and edema.

Table 9: Connective Tissue Tonics & Circulatory Stimulants
Botanical Key Clinical Indications Safety Concerns/Contraindications
Centella asiatica
(Gotu kola)
  • Vulnerary & Antioxidant which speeds wound healing, collagen formation, angiogenesis, and increases antioxidant levels within the wound in early stages of tissue repair while suppressing the formation of scar tissue.106-109
  • Promotes the repair of connective tissue (e.g. hair and nails, keloids, burns, scars, venous insufficiency and microangiopathy).110,111
  • Neuroprotective traditionally used to strengthen nervous system function & memory and bring stimulation to the brain via increased cerebral blood circulation.112-114
  • Side effects may include digestive upset, sedation, headaches, and photosensitization.
  • Allergic sensitivity in some patients.
  • May inhibit efficacy of anti-diabetic agents & anti-hyperlipidemics.
  • May have additive effects with vasodilators, CNS depressants, and alter effects of GABAergic medications.
Vaccinium myrtillus

(Bilberry)

  • Anti-inflammatory & vascular tonic for the treatment of peripheral vascular disorders & venous insufficiency including capillary fragility such as retinopathy hemorrhoids, and varicose veins.115,116
  • Improves microcirculation and lymph drainage in edema of the lower limbs, significantly reducing pain, sensation of heaviness, and swelling.117
  • Theoretically may cause hypotension, changes in blood sugar and digestive upset.
  • Use caution in hemorrhagic disorders, hypotension & hypoglycemia.
  • May interact with anti-diabetic agents & anti-hypertensives.
  • Potential additive effects with anti-coagulant medications.
Ginkgo biloba

(Ginkgo)

  • Antioxidant useful in peripheral vascular disease and restricted blood flow for any reason. Can inhibit platelet aggregation, relax blood vessels & improve their tone.118-120
  • Consider in impaired peripheral and cerebral circulation, heart disease, in the treatment and prevention of atherosclerosis, diabetes and metabolic syndrome, migraine, and physical symptoms of multiple sclerosis.121-126
  • Will help promote healing, particularly in peripheral tissues such as those in the arms and legs and in edematous conditions and disorders due to reduced retinal blood flow, normal tension glaucoma, age-related macular degeneration.127,128
  • Possible adverse reactions include headache, digestive upset and allergic dermatitis.
  • Avoid in history of bleeding or seizure disorder.
  • Use caution and monitor INR in patients on anti-platelet medications.
  • May potentiate antipsychotic medications in patients with schizophrenia and may induce hypomania in combination with SSRIs, MAOIs, trazadone, TCAs, buspirone, and St. John’s Wort.
  • May alter drug levels of some antiretroviral drugs, benzodiazepines, omeprazole, statins, hypoglycemics, tolbutamide, nifedipine & talinolol.
Crataegus spp.

(Hawthorn)

  • Protective towards blood vessel/endothelial tissue and connective tissue concerns (e.g. varicose veins, ulcers, and osteoporosis).129-131
  • Preventative of cardiovascular disease, having a beneficial effect on cardiac function and ability to reduce cardiovascular risk factors such as hypertension and thrombosis. May be used in heart failure (cardiac insufficiency), coronary artery disease, palpitations, arrhythmias, hypertension, atherosclerosis, hypercholesterolemia, angina, and weakness of the myocardium after infectious disease or ischemia.132-136
  • Use caution in severe hypotension.
  • In rare cases may cause digestive upset.
  • May inhibit effects of vasoconstrictors (e.g. Alpha-blockers) and decrease BP with nitrates & PDE-5 inhibitors (e.g. Sildenafil).
Aesculus hippocastanum

(Horse Chestnut)

  • Antioxidant and venous tonic which stimulates contraction of venous valves, increases venous pressure, supports lymphatic flow, improves and tones connective tissue & circulation.137-141
  • Will remove venous congestion and is indicated in acute thrombophlebitis, varicose veins, and hemorrhoids.142,143
  • May aid in swelling, bruising, fracture, and post traumatic injury of any kind. Was traditionally used as a topical application in neuralgic and rheumatic conditions.
  • High doses may cause digestive upset.
  • Avoid high or long-term doses, in children under 4, acute kidney inflammation, gastric ulcer, topical on broken or ulcerated skin.
  • Theoretical additive effects with antiplatelet medications.

 

Conclusions: A Herbal Approach to Healing Pain & Inflammation

Herbal medicine offers clinicians numerous possible remedies for addressing a multitude of pain & inflammatory syndromes. Though a symptomatic approach to pain relief may be useful, it is crucial to ensure healthy resolution of the inflammatory response, tissue repair, and regeneration. More appropriate and efficacious than treating symptoms with herbal medicine, is taking an individualized systems-based approach to treatment, removing the underlying cause whenever possible, and addressing contributing layers of disease (e.g. stress, anxiety, vascular disease) in order to slow tissue-damaging processes and maintain tissue function. An important note for clinicians is also to adequately educate patients regarding their expectations of the use of herbs as anti-inflammatories & analgesics. Herbs are not drugs, and thus their effects will not be as fast-acting. Herbs offer a long-term solution to resolution of inflammation and are capable of controlling uncomfortable symptoms while nourishing underlying tissue imbalances, however their effects are often dose-dependent, and depending on the severity of the condition may require more frequent dosing and re-evaluation.

Scientifically driven. Education focused. Healing Inspired.

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