Which is more damaging; Cannabis or Heroin? [split from DC]

[gloggawogga]

Paradoxcycle, the research you just posted, "temporary hippocampal lesions", was in animals, not human beings, and is only part of the drug's temporary effect. Now, please, put up or shut up, not this twisting of facts. Post case studies showing actual neurotoxic damage in human pot smokers, as we have done for herion addicts.

How is that relative to our discussion,

You made your use relevant to the discussion by bringing it up and using it as an example. You claimed above that heroin isn't more dangerous than pot "Because I am living proof that one can use heroin on a regular basis and maintain a "normal" life." But you need your wife to control your cravings. If you don't want me to comment on your use, don't use it as evidence in your argument. Sorry.

 

[paradoxcycle]

You need to step off glogga, you're way out of line.

There is sufficient evidence from human research to suggest that the cannabinoids act on the hippocampal region, producing behavioural changes similar to those caused by traumatic injury to that region. Human research has defined a pattern of acute CNS changes following cannabis administration; there is convincing evidence for long-lasting changes in brain function after long-term heavy use.

THC induces nuclear shrinkage and genomic DNA breakage in primary hippocampal neurons.



Binding of THC to cannabinoid CB1 receptors in hippocampal neurons leads to neuronal death. THC is neurotoxic at concentrations as low as 0.5-1.0 µM, which are comparable to THC levels measured in human plasma after consumption of marijuana

Furthermore, cannabinoids have been reported to stimulate cyclooxygenases (Reichman et al., 1987). The release of arachidonic acid and the subsequent generation of ROS in other systems are both implicated in cell damage (Kuehl and Egan, 1980) and cell death (Tang et al., 1996; Chen et al., 1997; Li et al., 1997; Wissing et al., 1997). ROS oxidizes membrane lipids, nucleic acids, and proteins, all of which can lead to necrotic or apoptotic cell death. Interestingly, THC causes DNA strand breaks, nuclear contraction, and cell body shrinkage, which are characteristic of cells undergoing apoptosis (Hockenbery, 1995; Majno and Joris, 1995).

Signaling pathways contributing to THC-induced neuronal death. It is hypothesized that excessive stimulation of cannabinoid receptors (CB1) by THC stimulates the production of arachidonic acid (AA) by several pathways. Cyclooxygenase (COX) catalyzes the formation of prostaglandins (PGs), thromboxanes (TXs), and reactive oxygen species (ROS), which stimulates peroxidation of lipids, proteins, and DNA. In addition, cannabinoid-induced transcriptional events may also contribute to THC induction of neuron death.


Treatment of hippocampal neurons with THC induces transcriptionally dependent cell death. This suggests that memory loss associated with marijuana treatment of humans, may be attributable to THC neurotoxicity.

 

[Morrison's Lament]

This has to be the most thoroughly referenced flamewar of all time

I'm just waiting for:

"Fuck you and your dirty whore of a mother!!!" (Harrington, 1967, p.29)

--- G.

 

[paradoxcycle]

I don't consider it a flamewar at all; I just don't understand why he feels the need to resort to personal insults. As I've said before, I like him

 

[Morrison's Lament]

I guess I just needed a vehicle for that joke

Very interesting discussion btw. While I'm not entirely convinced by your whole line of reasoning I am very sympathetic to the view that heroin problems are largely socially constructed through a perverse self-fulfilling prophecy afforded to it by it's status as the ultimate evil.

Research propasal: Find a bunch of pygmies in Africa, give them heroin, instruct them in it's use and tell them it's beneficial in small infrequent doses and dangerous in large or daily doses. Chart their progress, compare to people raised believing they are giving up their life with the first injection - award Nobel prize as appropriate

--- G.

 

[gloggawogga]

You need to step off glogga, you're way out of line.

There is sufficient evidence from human research

Bull shit. None of the research you are posting is on live human beings. The heroin brain lesions are in live human beings. You are in complete denial.

 

[paradoxcycle]

^
Uh....

Originally posted by paradoxcycle
There is sufficient evidence from human research to suggest that the cannabinoids act on the hippocampal region, producing behavioural changes similar to those caused by traumatic injury to that region. Human research has defined a pattern of acute CNS changes following cannabis administration; there is convincing evidence for long-lasting changes in brain function after long-term heavy use.

Originally posted by paradoxcycle
One of the primary effects in humans is the disruption of short-term memory, which is consistent with the abundance of CB1 receptors on the hippocampus.

Originally posted by paradoxcycle
Several laboratories have reported that chronic exposure to delta-9-tetrahydrocannabinol (THC) or marijuana extracts persistently altered the structure and function of the rat hippocampus, a paleocortical brain region involved with learning and memory processes in both rats and humans.

Originally posted by paradoxcycle
THC can be neurotoxic in humans & cannabis use is associated with neuronal loss.

 

[gloggawogga]

^^^^

Now you're posting someone's purely speculative interpretation of the research, and without any solid references, and as usual, none of the research you are posting is showing any actual nuerotoxicity in actual human subjects. Rats and cell cultures are not live human beings. Studies on acute intoxiciation, short term memory loss, etc., are not studies on nuerotoxicity. I want to see case studies on actual human beings showing neuronal damage, just like we have showing damage in heroin addicts, meth heads, etc. Can you do that? Post them. If you don't have case studies on actual humans being damaged, you haven't got much evidence that people need to worry that much.

 

[Morrison's Lament]

Just playing devil's advocate here, but who gives a fuck? We all know neurotoxicity is a neglible influence on the overall destructive influence of any given drug (except, perhaps, meth).

This hairsplitting is in reality totally irrelevant to the larger debate it presumes to address: the destructive properties of cannabis vs. the same properties of heroin. It's intellectual masturbation, and references are your porn

--- G.

 

[gloggawogga]

^^^^

Well yeah except the real human being case studies of toxic leucoencephalopathy and lesions in heroin users do look pretty bad. The evidence points to an unknown impurity, however. So you prolly only need to worry if you are doing street heroin. Pharmecuetical grade herion should be fine.

 

[paradoxcycle]

Originally posted by gloggawogga

Now you're posting someone's purely speculative interpretation of the research, and without any solid references, and as usual, none of the research you are posting is showing any actual nuerotoxicity in actual human subjects.

I cited actual research 8 or 10 times from legitimate sources!! And I even made separate posts on this page that used human subjects! HUMAN NUEROTOXICITY WAS MENTIONED AT LEAST A DOZEN TIMES.

Can you do that? Post them. If you don't have case studies on actual humans being damaged, you haven't got much evidence that people need to worry that much.

I did indeed post that.

Originally posted by Morrison's Lament

This hairsplitting is in reality totally irrelevant to the larger debate it presumes to address:

I mean, seriously, how long are you going to piss and moan about this? I am done with this thread. You have an unbelievable penchant for arguing; like the little boy in school who corrected the teachers simply because he could. 8(

 

[Blowmonkey]

Everyone has posted legitimate sources from legitimate researchers but you can't claim any of them being more conclusive as another, that's over simplistic.

I've edited the title slightly btw, describes the topic at hand a bit more accurately IMO.

 

[gloggawogga]

I cited actual research 8 or 10 times from legitimate sources!! And I even made separate posts on this page that used human subjects! HUMAN NUEROTOXICITY WAS MENTIONED AT LEAST A DOZEN TIMES.

You did not post any studies demonstrating any actual neurotoxicity in human subjects. You don't even seem to understand what I'm asking for. I'm asking for case studies on actual human beings showing actual damage, not speculations based on rat and test tube data.

These are examples of case studies onactual human beings showing actual damage:

Rev Neurol (Paris). 2002 Feb;158(2):177-82. Related Articles, Links
Click here to read
[Vacuolar leucoencephalopathy induced by heroin: 4 cases]

[Article in French]

Koussa S, Zabad R, Rizk T, Tamraz J, Nasnas R, Chemaly R.

Service de Neurologie, Hospital Hotel-Dieu de France, Faculte de Medicine, Beyrouth, Liban. [email protected]

We report 4 cases of toxic leucoencephalopathy after heroin inhalation. The clinical features, which usually occur some days or even longer after the last heroin consumption, are dominated by a cerebellar syndrome. The cerebellar hemispheres are almost always affected; the cerebral hemispheres, the cerebellar peduncles and the pyramidal tract may be affected. Vacuolar demyelination is the morphological substract of the lesions, which are symmmetrical, not contrast enhancing, hypodense on CT scan and hyperintense on T2-weighted MRI. The pathophysiology is unknown and seems different from post-anoxic leucoencephalopathy. The disease is usually progressive leading sometimes to death, but some cases show slow recovery.

Note they are talking about real damage in 4 real human beings, after heroin inhalation.

Di Yi Jun Yi Da Xue Xue Bao. 2002 Jul;22(7):659-60. Related Articles, Links

Single photon emission computerized tomography of spongiform leukoencephalopathy heroin addicts: analysis of 10 cases.

Wang Q, Lu BX.

Department of Neurology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China.

OBJECTIVE: To investigate the changes in cerebral circulation in heroin addicts with pongiform leukoencephalopathy. METHODS: Single photon emission computerized tomography (SPECT) was performed in 10 such patients. RESULTS: Regional cerebral blood flow (rCBF) in the involved white matter of bilateral cerebral and cerebellar hemispheres was obviously reduced. rCBF of temporal lobes, parietal lobes, cerebellar hemispheres and basal ganglion were reduced in varying degrees. CONCLUSION: As demonstrated by the result of SPECT, rCBF in the white matter of bilateral cerebral and cerebellar hemispheres was reduced with partial involvement of the gray matter of heroin addicts with spongiform leukoencephalopathy.

This is summary of 10 case studies, i.e. 10 actual heroin using actual human beings with actual damage

Chin Med J (Engl). 2001 Nov;114(11):1193-5. Related Articles, Links
Click here to read
Characteristics of spongiform leukoencephalopathy induced by heroin: MRI detection.

Zheng W, Zhang X.

Department of Diagnostic Radiology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China. [email protected]

OBJECTIVE: To elucidate the imaging characteristics of spongiform leukoencephalopathy induced by heroin and the diagnostic value of MRI examination. METHODS: Eleven cases of heroin addiction were examined by MRI. The sequences included T1-weighted imaging (T1WI), T2-weighted imaging (T2WI) and fast fluid-attenuated inversion recovery pulse sequence (Flair). RESULTS: Bilateral symmetrical lesions were located in the white matter of the cerebrum and cerebellum, the internal capsule in all cases, and the callosum in 6 cases. Elliptical lesions in the mesencephalon were found in two cases. These lesions were shown as hypointense signals on T1WI and hyperintense signals on T2WI and Flair's imaging. Cerebellar white matter suffered more severely, but the dentate nuclei were not invaded. CONCLUSION: Heroin-induced spongiform leukoencephalopathy has characteristic patterns in MRI, which are very specific to this form of the disease.

This is a study on 11 actual human subjects who were using heroin, who had actual damage

Acta Neuropathol (Berl). 1997 Jul;94(1):87-90. Related Articles, Links
Click here to read
Delayed spongiform leukoencephalopathy after heroin abuse.

Rizzuto N, Morbin M, Ferrari S, Cavallaro T, Sparaco M, Boso G, Gaetti L.

Department of Neurological and Visual Sciences, Policlinico Borgo Roma, University of Verona, Italy. [email protected]

Here we report the clinical and pathological findings in a 30-year-old drug addict in whom an intravenous injection of heroin led to reversible coma with respiratory depression and heart failure. On regaining consciousness, the patient was found to have rhabdomyolysis with renal failure requiring dialysis and peripheral neuropathy. Three weeks later his neurological condition suddenly deteriorated and delayed encephalopathy developed, leading to death 20 days later. The neuropathological study of the brain disclosed pale, spongy myelin with diffuse reactive astrogliosis and microglial proliferation, without hypoxic necrotic lesions. The cerebral and cerebellar cortices were unchanged. The absence of typical hypoxic lesions and the presence of spongiosis with massive astrocytosis distinguished this case from the previously reported cases of delayed leukoencephalopathy following severe hypoxia. An immunocytochemical study designed to exclude an underlying alteration of the metabolic oxidative pathway detected normal expression of the respiratory chain complexes IV, III and V. Despite the absence of an oxidative chain alteration in our patient, we cannot exclude the possibility that an individual predisposition played a pathogenetic role in this delayed leukoencephalopathy.

This is another case study on an actual human being who was using heroin, who suffered actual damage

[Leukoencephalopathy following inhalation of heroin pyrolysate]

[Article in German]

Hungerbuhler H, Waespe W.

Neurologische Klinik, Kantonsspital Aarau.

Inhalation of pre-heated heroin ("chinese blowing") is known to cause a spongiform leukoencephalopathy with marked neurological deficits. We report on 2 patients who developed severe cerebellar symptoms several days after interruption of heroin inhalation. The MRI findings suggested myelin damage to fibre tracts in the central nervous system, which are specifically involved in this disorder. Both patients survived with severe cerebellar deficits.

This is a case study on 2 actual human beings who were using heroin with actual damage

Leukoencephalopathy and raised brain lactate from heroin vapor inhalation ("chasing the dragon")

Kriegstein AR, Shungu DC, Millar WS, Armitage BA, Brust JC, Chillrud S, Goldman J, Lynch T.

Department of Neurology, Columbia University, College of Physicians and Surgeons, New York, NY, USA.

BACKGROUND: Inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy. METHODS: We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome. RESULTS: Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. Brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. Brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in Patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS. CONCLUSIONS: Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.

This one on 3 actual human beings who were using heroin, 2 of whom had actual damage.

Zhonghua Nei Ke Za Zhi. 2001 Nov;40(11):753-6. Related Articles, Links

[Clinical and pathological characteristics of heroin spongiform leukoencephalopathy in China]

[Article in Chinese]

Lu B, Zhou L, Pan S.

Department of Neurology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China.

OBJECTIVE: To observe the clinical, image and pathological characteristics of Heroin Spongiform Leukoencephalopathy(HSLE). METHODS: Clinical, CT and MRI analysis of 28 cases, brain autopsies of 2 cases and brain biopsies of 8 cases with HE, Loyez and Congo Red staining and observation through electron microscope. RESULTS: The clinic, image and pathologic characteristics of HSLE: (1) the history of inhalation of heated heroin vapor; (2) among 28 cases with HSLE, recurrence of HSLE was found in 17 cases during the abstinence, in 8 cases 1-2 month after abstinence, in 2 cases 4 month after abstinence and in 1 case after inhaling large amount of heroin; (3) the majority of cases were described with the acute onset characterized by cerebellar signs; (4) pyramidal tract lesion was frequently involved, but sensory system usually remained normal; (5) CSF test was normal; (6) CT and MRI revealed extensive symmetric white matter lesions in cerebra and cerebellum; (7) spongiform vacuoles degeneration of white matter was the main morphological change. CONCLUSIONS: Spongiform leukoencephalopathy may be considered if a patient who had a history of inhaling heated heroin vapor showed acute cerebellar signs. Spongiform vacuoles degeneration of cerebral white matter was the main pathological change.

This one on 28 actual human beings who were using heroin with actual damage

Eur Radiol. 1998;8(5):749-55. Related Articles, Links
Click here to read
Toxic spongiform leucoencephalopathy after inhaling heroin vapour.

Weber W, Henkes H, Moller P, Bade K, Kuhne D.

Klinik fur Allgemeine Rontgendiagnostik und Neuroradiologie, Alfried-Krupp-Krankenhaus, Alfried Krupp Strasse 21, D-45117, Essen, Germany.

This is a report of clinical, CT and MRI findings in a patient with toxic spongiform leucoencephalopathy after heroin ingestion. The disease is observed in drug addicts who inhale pre-heated heroin. The clinical onset, which usually occurs some days or even longer after the last heroin consumption, is characterized by a cerebellar syndrome. The cerebellar hemispheres, the cerebellar and cerebral peduncles and the pyramidal tract may be affected. Spongiform demyelination is the morphological substrate of the lesions, which are not contrast enhancing, hypodense on CT and hyperintense on T2-weighted MRI. The frequently perfect symmetry of the affection of functional systems points to a toxic and/or metabolic pathophysiological mechanism.

This one on 1 actual human being, with actual damage

Arch Anat Cytol Pathol. 1996;44(1):12-7. Related Articles, Links

[Cerebral infarctions in a drug addict inhaling heroin]

[Article in French]

Adle-Biassette H, Marc B, Benhaiem-Sigaux N, Durigon M, Gray F.

Departement de Pathologie, Hopital Henri Mondor, CRETEIL.

Cerebral infarcts complicating heroin abuse have been seldom reported and only clinically and radiologically documented. We report a pathological case of cerebral infarct in a heroin sniffer. A 31 year old, male, heroin sniffing addict for several years, with no known past neurological history, was found dead one morning. The evening before, he had presented the usual signs of recent heroin intake. Opiates were found in large amounts in blood and urine. Post mortem HIV serology was negative. Post mortem examination revealed the usual signs of heroin addiction, but no cutaneous signs of IV drug use. Myocardial ischemic lesions of various ages involved the anterolateral part of the left ventricle; coronary arteries were normal. Neuropathological study revealed, partly cystic infarcts involving both cerebral hemispheres. They were mostly cortical with an intralaminar pattern and a watershed distribution at the boundaries between the territories of the anterior and middle cerebral arteries and the middle posterior cerebral arteries. Intracerebral vessels, large intracranial and cervical arteries were normal.

Another one on 1 actual human subject with actual damage

Acute leukoencephalopathy after inhalation of a single dose of heroin.

Vella S, Kreis R, Lovblad KO, Steinlin M.

Division of Child Neurology, Inselspital, Bern, Switzerland. [email protected]

We describe extended and repeat magnetic resonance (MR) examinations in the case of a 16-year-old male who developed acute left-sided sensorimotor hemiplegia after a single dose of inhaled heroin. MRI revealed symmetrical hyperintense signals in T 2 -weighted images and massive diffusion disorders in the diffusion weighted images predominantly in parieto-occipital subcortical white matter and both ventral globi pallidi with preservation of U fibers and no brain oedema. MR spectroscopy data were compatible with combined hypoxic and mitochondrial damage resulting in axonal injury without demyelination. Normal values and variations had been obtained from spectra of five age-matched subjects. This is the first reported MR follow-up study of leukoencephalopathy occurring acutely after a first inhaled dose of heroin. We postulate that toxic spongiform leukoencephalopathy in heroin addicts may be the outcome of a complex mechanism directly triggered by heroin and causing mitochondrial as well as hypoxic injury in specific and limited areas of white matter.

This on a 16 year old actual human subject who allegedely had only one dose and suffered actual damage

Arch Neurol. 2003 Nov;60(11):1605-6. Related Articles, Links
Click here to read
Symmetric deep cerebellar lesions after smoking heroin.

Ropper AH, Blair R.

Neurology Service and Department of Radiology, St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA. [email protected]

BACKGROUND: Acute symmetric deep cerebellar lesions suggest toxic exposure. OBJECTIVE: To describe a patient with striking neurologic and magnetic resonance image features. DESIGN: Case report. SETTING: Emergency department and office. METHODS: Personal observation. RESULTS: A middle-aged man had a day of unsteadiness, followed by acute and pronounced cerebellar signs. The degree of disability was remarkable. Magnetic resonance imaging showed almost perfectly symmetric deep cerebellar damage that ultimately became cavitated. Serial querying of the patient revealed the use of heroin by inhalation just prior to the emergence of the ataxic syndrome. CONCLUSIONS: An acute and purely ataxic syndrome with symmetric deep cerebellar lesions suggests toxic exposure, in this case, the smoking of heroin.

Another study on an actual damage on an actual human subject who had recently been using heroin.






<....pays homage to the "will he understand" god.....>


Now what I want to see, Paradoxcycle, is studies like these but with THC/cannabis users not heroin users. Do you understand what I'm asking for? If THC/cannabis were damaging people's brains, there would be this sort of evidence, as hundreds of millions or so around the world use cannabis.

 

[gloggawogga]

You have an unbelievable penchant for arguing; like the little boy in school who corrected the teachers simply because he could.

Allright. Now who is being personal? If you don't want me to be personal, Paradoxcycle, don't bait me.

 

[Pimp Lazy]

Whoa… dude… wasn't this mentioned before? I was under the distinct impression that heroin-use induced (heh heh) leukodystrophy was a direct result from smoking an adulterant. I've got a serious question though in regards to whether brain damage from heroin is a realistic concern from methods other than smoking. It seems that cardiac or pulmonary disfunction would be of more concern. Does anyone use heroin for 50 years? Because people use cannabis for that long.

"Damn Grand-dad! Take it easy and pass that joint."
"I taught Bogart everything he knew."

Peace.

 

[RollinWitAcoldBilly]

So you tell us heroin is no more dangerous than pot yet you need another person to control your own craving for heroin. Obviously, your passion for the drug is strong enough you can't think objectively about it either.

I agree.

 

[RollinWitAcoldBilly]

So you're turning this into a personal attack now? You're setting a great example, glogga. I have no interest in continuing this discussion if you feel the need to resort to this.

Hes not talking shit to you dude. You sound very biased, honestly. It seems like your love of opiates has blinded you a little bit. Just seems that way..

 

[supersnail]

Paradoxcycle, you've posted a whole bunch of stuff, none of which satisfies the criteria gloggawogga or I am looking for.

You have yet to show us a study that:
1. is an actual research study, not a textbook author's interpretation of primary research.
2. demonstrates neurotoxicity in humans, not in cultured cells
3. demonstrates a lasting neurotoxicity, which in the case of heavy users means one that persists months after they've ceased use, when it's certain that observed effects are not just lingering acute ones.

even if you are able to dig up such a study, or two, i have already linked a couple review articles that describe forty studies that have found no evidence of cannabis neurotoxicity.

as far as i can tell, the current consensus among the research community is that cannabis has no lasting neurotoxic effects in humans.

your evidence has yet to cast any significant doubt on that statement.

 

[paradoxcycle]

Just a heads-up:

1) I never requested this thread to be moved to CD, the original topic was is THC neurotoxic and now the thread is Which is more damaging; Cannabis or Heroin?!!?

2) It's unfair that I have already proven THC is neurotoxic and you all demand that I continue to cite studies regarding heroin neurotoxicity.

I've proven my point previously, so I'm done with this thread. It's disheartening that you've all decided to join forces against me (especially considering one of you is a mod). Of course you will all assert cannabis is a safer drug, look what forum we're in. This whole thing has turned into a childish "no, I'm right, you're wrong, no, I'm right, you're wrong" dispute and I don't have the time to continue it.

 

[awatkins]

i think the original poster was misunderstood in the first place, he refers to some things as soft drugs but that doesn't mean he thinks they are harmless, i think when he said soft drugs, i think he was talking about cultures' expectations of what a "soft drug" is which would be pot;-not because it actually is a soft drug but rather that the culture views pot this way
he is referring to people that do soft drugs that compare their drug to other "harder drugs" in order to validate their own drug use and like the original poster said they dont' see the damage done to themselves,

so if anything, paradoxcycle, the original poster DID imply that pot is harmful, assuming that pot is a "soft drug",
i personally think "soft drug" is a bullshit term
saying that "pot is my heroin" means the same thing as "heroin is my pot"as far as i am concerned